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2 - Keiser A&P 2 > 0-1 Chapter 19 the heart > Flashcards

0-1 Chapter 19 the heart Flashcards

1
Q

cardiology

A

the scientific study of the heart and the treatment of its disorders

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2
Q

cardiovascular system

A

heart and blood vessels

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3
Q

circulatory system

A

heart, blood vessels, and the blood

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4
Q

major divisions of circulatory system

A

pulmonary circuit

systemic circuit

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5
Q

pulmonary circuit

A

right side of heart
•carries blood to lungs for gas exchange and back to hear
–lesser oxygenated blood arrives from inferior and superior vena cava
–blood sent to lungs via pulmonary trunk

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6
Q

systemic circuit

A

left side of heart
•supplies oxygenated blood to all tissues of the body and returns it to the heart
–fully oxygenated blood arrives from lungs via pulmonary veins
–blood sent to all organs of the body via aorta

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7
Q

Heart

A

heart located in mediastinum, between lungs

tilted to the left

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8
Q

base

A

wide, superior portion of heart, blood vessels attach here

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9
Q

apex

A

inferior end, tilts to the left, tapers to point

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10
Q

pericardium

A

double-walled sac (pericardial sac) that encloses the heart
–allows heart to beat without friction, provides room to expand, yet resists excessive expansion
–anchored to diaphragm inferiorly and sternum anteriorly

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11
Q

parietal pericardium

A

outer wall of sac
–superficial fibrous layer of connective tissue
–a deep, thin serous layer

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12
Q

visceral pericardium

A

(epicardium) –heart covering

–serous lining of sac turns inward at base of heart to cover the heart surface

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13
Q

pericardial cavity

A

space inside the pericardial sac filled with 5 -30 mL of pericardial fluid

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14
Q

pericarditis

A

inflammation of the membranes

–painful friction rub with each heartbeat

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15
Q

epicardium

A

(visceral pericardium)
–serous membrane covering heart
–adipose in thick layer in some places
–coronary blood vessels travel through this layer

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16
Q

endocardium

A

–smooth inner lining of heart and blood vessels

–covers the valve surfaces and continuous with endothelium of blood vessels

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17
Q

myocardium

A

layer of cardiac muscle proportional to work load

•muscle spirals around heart which produces wringing motion

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18
Q

fibrous skeleton of the heart

A

-framework of collagenous and elastic fibers
•provides structural support and attachment for cardiac muscle and anchor for valve tissue
•electrical insulation between atria and ventricles important in timing and coordination of contractile activity

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19
Q

four chambers

A

right and left atria

right and left ventricles

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20
Q

right and left atria

A
  • two superior chambers
  • receive blood returning to heart
  • auricles (seen on surface) enlarge chamber
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21
Q

right and left ventricles

A

two inferior chambers

•pump blood into arteries

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22
Q

atrioventricular sulcus

A
  • separates atria and ventricles

- sulci contain coronary arteries

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23
Q

interventricular sulcus

A
  • overlies the interventricular septum that divides the right ventricle from the left
  • sulci contain coronary arteries
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24
Q

interatrial septum

A

–wall that separates atria

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25
Q

pectinate muscles

A

internal ridges of myocardium in right atrium

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26
Q

interventricular septum

A

muscular wall that separates ventricles

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27
Q

trabeculae carneae

A

internal ridges in both ventricles

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28
Q

Heart Valves

A

valves ensure a one-way flow of blood through the heart

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29
Q

atrioventricular (AV) valves

A

controls blood flow between atria and ventricles
–right AV valve has 3 cusps (tricuspid valve)
–left AV valve has 2 cusps (mitral or bicuspid valve)

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30
Q

chordae tendineae

A

cords connect AV valves to papillary muscles on floor of ventricles
•prevent AV valves from flipping inside out or bulging into the atria when the ventricles contract

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31
Q

tricuspid valve

A

right AV valve has 3 cusps (tricuspid valve)

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32
Q

bicuspid valve

A

left AV valve has 2 cusps (mitral or bicuspid valve)

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33
Q

semilunar valves

A

control flow into great arteries –open and close because of blood flow and pressure

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34
Q

pulmonary semilunar valve

A

in opening between right ventricle and pulmonary trunk

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35
Q

aortic semilunar valve

A

in opening between left ventricle and aorta

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36
Q

AV Valve Mechanics

ventricles relax

A

–pressure drops inside the ventricles
–semilunar valves close as blood attempts to back up into the ventricles from the vessels
–AV valves open
–blood flows from atria to ventricles

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37
Q

AV Valve Mechanics

ventricles contract

A

–AV valves close as blood attempts to back up into the atria
–pressure rises inside of the ventricles
–semilunar valves open and blood flows into great vessels

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38
Q

Blood Flow Through Heart

part 1

A
  • Blood enters right atrium from superior and inferior venae cavae
  • Blood in right atrium flows through right AV valve into right ventricle
  • Contraction of right ventricle forces pulmonary valve open
  • Blood flows through pulmonary valve into pulmonary trunk
  • Blood is distributed by right and left pulmonary arteries to the lungs, where it unloads CO2 and loads O2.
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39
Q

Blood Flow Through Heart

part 2

A
  • Blood returns from lungs via pulmonary veins to left atrium
  • Blood in left atrium flows through left AV valve into left ventricle
  • Contraction of left ventricle (simultaneous with step 3 ) forces aortic valve open
  • Blood flows through aortic valve into ascending aorta
  • Blood in aorta is distributed to every organ in the body, where it unloads O2and loads CO2
  • Blood returns to heart via venae cavae
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40
Q

Coronary Circulation

A

5% of blood pumped by heart is pumped to the heart itself through the coronary circulation to sustain its strenuous workload
–250 ml of blood per minute
–needs abundant O2and nutrients

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41
Q

left coronary artery

A

(LCA) branch off the ascending aorta

  • anterior interventricular branch
  • circumflex branch
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42
Q

anterior interventricular branch

A

•supplies blood to both ventricles and anterior two-thirds of the interventricular septum

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43
Q

circumflex branch

A
  • passes around left side of heart in coronary sulcus
  • gives off left marginal branch and then ends on the posterior side of the heart
  • supplies left atrium and posterior wall of left ventricle
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44
Q

right coronary artery

A

RCA) branch off the ascending aorta

–supplies right atrium and sinoatrial node (pacemaker)

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45
Q

right marginal branch

A

•supplies lateral aspect of right atrium and ventricle

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46
Q

posterior interventricular branch

A

supplies posterior walls of ventricles

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47
Q

myocardial infarction

A

MI) (heart attack)
–interruption of blood supply to the heart from a blood clot or fatty deposit (atheroma) can cause death of cardiac cells within minutes
–some protection from MI is provided by arterial anastomoses which provides an alternative route of blood flow (collateral circulation) within the myocardium

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48
Q

blood flow to the heart muscle during ventricular contraction is

A

slowed, unlike the rest of the body

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49
Q

three reasons:

A

–contraction of the myocardium compresses the coronary arteries and obstructs blood flow
–opening of the aortic valve flap during ventricular systole covers the openings to the coronary arteries blocking blood flow into them
–during ventricular diastole, blood in the aorta surges back toward the heart and into the openings of the coronary arteries
•blood flow to the myocardium increases during ventricular relaxation

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50
Q

angina pectoris

A

chest pain from partial obstruction of coronary blood flow
–pain caused by ischemia of cardiac muscle
–obstruction partially blocks blood flow
–myocardium shifts to anaerobic fermentation producing lactic acid stimulating pain

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51
Q

myocardial infarction

A

sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation
–MI responsible for about half of all deaths in the United States

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52
Q

Venous Drainage of Heart

A

5 -10% drains directly into heart chambers, right atrium and right ventricle, by way of the thebesian veins

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53
Q

the rest returns to right atrium by the following routes:

A

great cardiac vein
middle cardiac vein
left marginal vein

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54
Q

great cardiac vein

A
  • travels along side of anterior interventricular artery
  • collects blood from anterior portion of heart
  • empties into coronary sinus
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55
Q

middle cardiac vein

A

(posterior interventricular)
•found in posterior sulcus
•collects blood from posterior portion of heart
•drains into coronary sinus

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56
Q

left marginal vein

A

•empties into coronary sinus

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57
Q

coronary sinus

A
  • large transverse vein in coronary sulcus on posterior side of heart
  • collects blood and empties into right atrium
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58
Q

cardiocytes

A

striated, short, thick, branched cells, one central nucleus surrounded by light staining mass of glycogen

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59
Q

intercalated discs

A

join cardiocytes end to end

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60
Q

interdigitating folds

A

folds interlock with each other, and increase surface area of contact

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61
Q

mechanical junctions

A

tightly join cardiocytes

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62
Q

fascia adherens

A

broad band in which the actin of the thin myofilaments is anchored to the plasma membrane
–each cell is linked to the next via transmembrane proteins

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63
Q

desmosomes

A

weldlike mechanical junctions between cells

–prevents cardiocytes from being pulled apart

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64
Q

electrical junctions

A

gap junctions allow ions to flow between cells –can stimulate neighbors
•entire myocardium of either two atria or two ventricles acts like single unified cell

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65
Q

repair of damage of cardiac muscle is almost entirely by

A

fibrosis (scarring)

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66
Q

cardiac muscle depends almost exclusively on

A

aerobic respiration used to make ATP
–rich in myoglobin and glycogen
–huge mitochondria –fill 25% of cell

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67
Q

adaptable to organic fuels used

A 
fatty acids (60%), glucose (35%), ketones, lactic acid and amino acids (5%)
–more vulnerable to oxygen deficiency than lack of a specific fuel
PREFERS FAT
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68
Q

fatigue resistant

A

since makes little use of anaerobic fermentation or oxygen debt mechanisms
–does not fatigue for a lifetime

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69
Q

Cardiac Conduction System

A

coordinates the heartbeat
–composed of an internal pacemaker and nervelike conduction pathways through myocardium
–generates and conducts rhythmic electrical signals in the following order:

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70
Q

Cardiac Conduction System

Order

A

sinoatrial (SA) node
atrioventricular (AV) node
atrioventricular (AV) bundle (bundle of His)
Purkinje fibers

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71
Q

sinoatrial (SA) node

A

modified cardiocytes
–initiates each heartbeat and determines heart rate
–signals spread throughout atria
–pacemaker in right atrium near base of superior vena cava

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72
Q

atrioventricular (AV) node

A

–located near the right AV valve at lower end of interatrial septum
–electrical gateway to the ventricles
–fibrous skeleton acts as an insulator to prevent currents from getting to the ventricles from any other route

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73
Q

atrioventricular (AV) bundle (bundle of His)

A

–bundle forks into right and left bundle branches

–these branches pass through interventricular septum toward apex

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74
Q

Purkinje fibers

A

–nervelike processes spread throughout ventricular myocardium
•signal pass from cell to cell through gap junctions

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75
Q

Cardiac Conduction System

sequence

A
  • SA node fires
  • Excitation spreads through atrial myocardium
  • .AV node fires
  • Excitation spreads down AV bundle
  • Purkinje fibers distribute excitation through ventricular myocardium.
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76
Q

sympathetic nerves

A

(raise heart rate)
•increase heart rate and contraction strength
•dilates coronary arteries to increase myocardial blood flow

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77
Q

sympathetic nerves

path

A

–sympathetic pathway to the heart originates in the upper thoracic segments of the spinal cord
–continues to adjacent sympathetic chain ganglia
–some pass through cardiac plexus in mediastinum
–continue as cardiac nerves to the heart
–fibers terminate in SA and AV nodes, in atrial and ventricular myocardium, as well as the aorta, pulmonary trunk, and coronary arteries

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78
Q

parasympathetic nerves

A

(slows heart rate)

•parasympathetic stimulation reduces the heart rate

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79
Q

parasympathetic nerves

path

A

–pathway begins with nuclei of the vagus nerves in the medulla oblongata
–extend to cardiac plexus and continue to the heart by way of the cardiac nerves
–fibers of right vagus nerve lead to the SA node
–fibers of left vagus nerve lead to the AV node
–little or no vagal stimulation of the myocardium

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80
Q

systole

A

atrial or ventricular contraction

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81
Q

diastole

A

atrial or ventricular relaxation

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82
Q

sinus rhythm

A

normal heartbeat triggered by the SA node
–set by SA node at 60 –100 bpm
–adult at rest is 70 to 80 bpm (vagal tone)

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83
Q

ectopic focus

A

another parts of heart fires before SA node

–caused by hypoxia, electrolyte imbalance, or caffeine, nicotine, and other drugs

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84
Q

Abnormal Heart Rhythms

A

spontaneous firing from some part of heart not the SA node

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85
Q

ectopic foci

A

region of spontaneous firing

86
Q

nodal rhythm

A

if SA node is damaged, heart rate is set by AV node, 40 to 50 bpm

87
Q

intrinsic ventricular rhythm

A

if both SA and AV nodes are not functioning, rate set at 20 to 40 bpm
–this requires pacemaker to sustain life

88
Q

arrhythmia

A

any abnormal cardiac rhythm
–failure of conduction system to transmit signals (heart block)
•bundle branch block
•total heart block (damage to AV node)

89
Q

Cardiac Arrhythmias

A

atrial flutter
premature ventricular contractions
ventricular fibrillation

90
Q

atrial flutter

A

ectopic foci in atria
–atrial fibrillation
–atria beat 200 -400 times per minute

91
Q

premature ventricular contractions

A

–caused by stimulants, stress or lack of sleep

92
Q

ventricular fibrillation

A

–serious arrhythmia caused by electrical signals reaching different regions at widely different times
•heart can‟t pump blood and no coronary perfusion
–kills quickly if not stopped

93
Q

defibrillation

A

strong electrical shock whose intent is to depolarize the entire myocardium, stop the fibrillation, and reset SA nodes to sinus rhythm

94
Q

SA node

A

•SA node is the system‟s pacemaker

95
Q

SA node does not have a stable resting membrane potential

A

–starts at -60 mV and drifts upward from a slow inflow of Na+
•gradual depolarization is called pacemaker potential
–slow inflow of Na+ without a compensating outflow of K+
–when reaches threshold of -40 mV, voltage-gated fast Ca2+and Na+ channels open
•faster depolarization occurs peaking at 0 mV
•K+ channels then open and K+ leaves the cell
–causing repolarization
–once K+ channels close, pacemaker potential starts over

96
Q

each depolarization of the SA node sets off one heartbeat

A

one heartbeat

-at rest, fires every 0.8 seconds or 75 bpm

97
Q

Impulse Conduction to Myocardium

A
  • signal from SA node stimulates two atria to contract almost simultaneously
  • signal slows down through AV node
  • signals travel very quickly through AV bundle and Purkinje fibers
  • ventricular systole progresses up from the apex of the heart
98
Q

Electrical Behavior of Myocardium

A
  • cardiocytes have a stable resting potential of -90 mV

* depolarize only when stimulated

99
Q

depolarization phase

A

(very brief)
•stimulus opens voltage regulated Na+ gates, (Na+ rushes in) membrane depolarizes rapidly
•action potential peaks at +30 mV
•Na+ gates close quickly

100
Q

plateau phase

A

lasts 200 to 250 msec, sustains contraction for expulsion of blood from heart
•Ca2+ channels are slow to close and SR is slow to remove Ca2+ from the cytosol

101
Q

repolarization phase

A

Ca2+channels close, K+ channels open, rapid diffusion of K+ out of cell returns it to resting potential

102
Q

has a long absolute refractory period of

A

250 msec compared to 1 –2 msec in skeletal muscle

–prevents wave summation and tetanus which would stop the pumping action of the heart

103
Q

Action Potential of a Cardiocyte

A

1) Na+ gates open
2) Rapid depolarization
3) Na+ gates close, K+ channels begin to open
4) Slow Ca2+ channels open
5) Ca2+channels close, K+ channels fully open (repolarization)

104
Q

Electrocardiogram

A

(ECG or EKG)
•composite of all action potentials of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs and chest

105
Q

ECG Deflections

A

P wave
QRS complex
ST segment -ventricular systole
T wave

106
Q

P wave

A

–SA node fires, atria depolarize and contract

–atrial systole begins 100 msec after SA signal

107
Q

QRS complex

A

–ventricular depolarization

–complex shape of spike due to different thickness and shape of the two ventricles

108
Q

ST segment -ventricular systole

A

–plateau in myocardial action potential

109
Q

T wave

A

–ventricular repolarization and relaxation

110
Q

Electrical Activity of Myocardium

A

1) atrial depolarization begins
2) atrial depolarization complete (atria contracted)
3) ventricles begin to depolarize at apex; atria repolarize (atria relaxed)
4) ventricular depolarization complete (ventricles contracted)
5) ventricles begin to repolarize at apex
6) ventricular repolarization complete (ventricles relaxed)

111
Q

Diagnostic Value of ECG

A
  • abnormalities in conduction pathways
  • myocardial infarction
  • nodal damage
  • heart enlargement
  • electrolyte and hormone imbalances
112
Q

cardiac cycle

A

one complete contraction and relaxation of all four chambers of the heart

113
Q

atrial systole

A

(contraction) occurs while ventricles are in diastole(relaxation)

114
Q

atrial diastole

A

occurs while ventricles in systole

115
Q

quiescent period

A

all four chambers relaxed at same time

116
Q

two main variables that govern fluid movement:

A

pressure

resistance

117
Q

pressure

A

causes a fluid to flow (fluid dynamics)
–pressure gradient -pressure difference between two points
–measured in mm Hg with a manometer or sphygmomanometer

118
Q

resistance

A

opposes fluid flow
–great vessels have positive blood pressure
–ventricular pressure must rise above this resistance for blood to flow into great vessels

119
Q

Pressure Gradients and Flow

A

fluid flows only if it is subjected to more pressure at one point than another which creates a pressure gradient
–fluid flows down its pressure gradient from high pressure to low pressure

120
Q

events occurring on left side of heart

A

–when ventricle relaxes and expands, its internal pressure falls
–if bicuspid valve is open, blood flows into left ventricle
–when ventricle contracts, internal pressure rises
–AV valves close and the aortic valve is pushed open and blood flows into aorta from left ventricle

121
Q

opening and closing of valves are governed

A

by these pressure changes
–AV valves limp when ventricles relaxed
–semilunar valves under pressure from blood in vessels when ventricles relaxed

122
Q

valvular insufficiency

A

(incompetence) -any failure of a valve to prevent reflux (regurgitation) the backward flow of blood

123
Q

valvular stenosis

A

cusps are stiffened and opening is constricted by scar tissue
•result of rheumatic fever autoimmune attack on the mitral and aortic valves
•heart overworks and may become enlarged

124
Q

heart murmur

A

–abnormal heart sound produced by regurgitation of blood through incompetent valves

125
Q

mitral valve prolapse

A

insufficiency in which one or both mitral valve cusps bulge into atria during ventricular contraction
•hereditary in 1 out of 40 people
•may cause chest pain and shortness of breath

126
Q

auscultation

A

listening to sounds made by body

127
Q

first heart sound

A

(S1), louder and longer “lubb”, occurs with closure of AV valves, turbulence in the bloodstream, and movements of the heart wall

128
Q

second heart sound

A

(S2), softer and sharper “dupp” occurs with closure of semilunar valves, turbulence in the bloodstream, and movements of the heart wall

129
Q

Phases of Cardiac Cycle

A
  • ventricular filling
  • isovolumetric contraction
  • ventricular ejection
  • isovolumetric relaxation
130
Q

Ventricular Filling

A

during diastole, ventricles expand
–their pressure drops below that of the atria
–AV valves open and blood flows into the ventricles

131
Q

ventricular filling occurs in three phases:

A

rapid ventricular filling
diastasis
atrial systole

132
Q

rapid ventricular filling

A

first one-third

•blood enters very quickly

133
Q

diastasis

A

second one-third
•marked by slower filling
•P wave occurs at the end of diastasis

134
Q

atrial systole

A

final one-third

•atria contract

135
Q

end-diastolic volume

A

(EDV) –amount of blood contained in each ventricle at the end of ventricular filling
–130 mL of blood

136
Q

Isovolumetric Contraction

A

atria repolarize and relax
ventricles depolarize
AV valves close
heart sound S1

137
Q

atria repolarize and relax

A

–remain in diastole for the rest of the cardiac cycle

138
Q

ventricles depolarize

A

create the QRS complex, and begin to contract

139
Q

AV valves close

A

as ventricular blood surges back against the cusps

140
Q

heart sound S1

A

occurs at the beginning of this phase

141
Q

isovolumetric‟

A

because even though the ventricles contract, they do not eject blood
–because pressure in the aorta (80 mm Hg) and in pulmonary trunk (10 mm Hg) is still greater than in the ventricles

142
Q

cardiocytes exert force, but

A

but with all four valves closed, the blood cannot go anywhere

143
Q

Ventricular Ejection

A

•ejection of blood begins when the ventricular pressure exceeds arterial pressure and forces semilunar valves open
–pressure peaks in left ventricle at about 120 mm Hg and 25 mm Hg in the right

144
Q

rapid ejection

A

blood spurts out of each ventricle rapidly at first

145
Q

reduced ejection

A

then more slowly under reduced pressure

146
Q

ventricular ejections last

A

about 200 –250 msec

–corresponds to the plateau phase of the cardiac action potential

147
Q

T wave occurs

A

late in this phase

148
Q

stroke volume (SV)

A

of about 70 mL of blood is ejected of the 130 mL in each ventricle

149
Q

ejection fraction

A

of about 54%

–as high as 90% in vigorous exercise

150
Q

end-systolic volume (ESV

A

the 60 mL of blood left behind

151
Q

Isovolumetric Relaxation

A

early ventricular diastole

–when T wave ends and the ventricles begin to expand

152
Q

elastic recoil and expansion would cause pressure to drop rapidly and suck blood into the ventricles

A

–blood from the aorta and pulmonary artery briefly flows backwards
–filling the semilunar valves and closing the cusps
–creates a slight pressure rebound that appears as the dicrotic notch of the aortic pressure curve
–heart sound S2occurs as blood rebounds from the closed semilunar valves and the ventricle expands
–„isovolumetric‟ because semilunar valves are closed and AV valves have not yet opened
•ventricles are therefore taking in no blood

153
Q

when AV valves open

A

ventricular filling begins again

154
Q

Timing of Cardiac Cycle

in a resting person

A

–atrial systole last about 0.1 sec
–ventricular systole about 0.3 sec
–quiescent period, when all four chambers are in diastole, 0.4 sec

155
Q

total duration of the cardiac cycle is

A

therefore 0.8 sec in a heart beating 75 bpm

156
Q

Overview of Volume Changes

A

end-systolic volume (ESV)60 ml
-passively added to ventricle during atrial diastole+30 ml
-added by atrial systole+40 ml
total: end-diastolic volume (EDV) 130 ml
stroke volume (SV) ejected by ventricular systole-70 ml
leaves: end-systolic volume (ESV)60 ml
both ventricles must eject same amount of blood

157
Q

Unbalanced Ventricular Output

pulmonary edema

A 
-Right ventricular output exceeds left
ventricular output.
-Pressure backs up
-Fluid accumulates in
pulmonary tissue
158
Q

Unbalanced Ventricular Output

peripheral edema

A 
-Left ventricular output exceeds right
ventricular output.
-Pressure backs up
-Fluid accumulates in
systemic tissue
159
Q

congestive heart failure

A

(CHF) -results from the failure of either ventricle to eject blood effectively
–usually due to a heart weakened by myocardial infarction, chronic hypertension, valvular insufficiency, or congenital defects in heart structure.
-eventually leads to total heart failure

160
Q

left ventricular failure

A

blood backs up into the lungs causing pulmonary edema

–shortness of breath or sense of suffocation

161
Q

right ventricular failure

A

blood backs up in the vena cava causing systemic or generalized edema
–enlargement of the liver, ascites (pooling of fluid in abdominal cavity), distension of jugular veins, swelling of the fingers, ankles, and feet

162
Q

cardiac output

A

(CO) –the amount ejected by ventricle in 1 minute

163
Q

cardiac output =

A

cardiac output = heart rate x stroke volume
–about 4 to 6 L/min at rest
–a RBC leaving the left ventricle will arrive back at the left ventricle in about 1 minute
–vigorous exercise increases CO to 21 L/min for fit person and up to 35 L/min for world class athlete

164
Q

cardiac reserve

A

the difference between a person‟s maximum and resting CO

–increases with fitness, decreases with disease

165
Q

pulse

A

surge of pressure produced by each heart beat that can be felt by palpating a superficial artery with the fingertips

166
Q

pulse rates

A

–infants have HR of 120 bpm or more
–young adult females avg. 72 -80 bpm
–young adult males avg. 64 to 72 bpm
–heart rate rises again in the elderly

167
Q

tachycardia

A

resting adult heart rate above 100 bpm
–stress, anxiety, drugs, heart disease, or fever
–loss of blood or damage to myocardium

168
Q

bradycardia

A

resting adult heart rate of less than 60 bpm

–in sleep, low body temperature, and endurance trained athletes

169
Q

positive chronotropic agents

A

factors that raise the heart rate

170
Q

negative chronotropic agents

A

factors that lower heart rate

171
Q

Chronotropic Effects of the Autonomic Nervous System

A
  • autonomic nervous system does not initiate the heartbeat, it modulates rhythm and force
  • cardiac centers in the reticular formation of the medulla oblongata initiate autonomic output to the heart
172
Q

cardiostimulatory effect

A

some neurons of the cardiac center transmit signals to the heart by way of sympathetic pathway

173
Q

cardioinhibitory effect

A

others transmit parasympathetic signals by way of the vagus nerve

174
Q

sympathetic postganglionic fibers are adrenergic

A

–they release norepinephrine
–binds to β-adrenergic fibers in the heart
–activates c-AMP second-messenger system in cardiocytes and nodal cells
–leads to opening of Ca2+ channels in plasma membrane
–increased Ca2+ inflow accelerated depolarization of SA node
–cAMP accelerates the uptake of Ca2+ by the sarcoplasmic reticulum allowing the cardiocytes to relax more quickly
–by accelerating both contraction and relaxation, norepinephrine and cAMP increase the heart rate as high as 230 bpm
–diastole becomes too brief for adequate filling
–both stroke volume and cardiac output are reduced

175
Q

parasympathetic vagus nerves have cholinergic, inhibitory effects on the SA and AV nodes

A

–acetylcholine (ACh) binds to muscarinic receptors
–opens K+ gates in the nodal cells
–as K+leaves the cells, they become hyperpolarized and fire less frequently
–heart slows down
–parasympathetics work on the heart faster than sympathetics
•parasympathetics do not need a second messenger system

176
Q

without influence from the cardiac centers, the heart has a intrinsic ―natural‖ firing rate

A

of 100 bpm

177
Q

vagal tone

A

holds down this heart rate to 70 –80 bpm at rest

–steady background firing rate of the vagus nerves

178
Q

cardiac centers in the medulla

A

receive input from many sources and integrate it into the „decision‟ to speed or slow the heart

179
Q

higher brain centers

A

affect heart rate
–cerebral cortex, limbic system, hypothalamus
•sensory or emotional stimuli

180
Q

proprioceptors in the muscles and joints

A

inform cardiac center about changes in activity, HR increases before metabolic demands of muscle arise

181
Q

baroreceptors signal cardiac center

A
  • pressure sensors in aorta and internal carotid arteries
  • blood pressure decreases, signal rate drops, cardiac center increases heart rate
  • if blood pressure increases, signal rate rises, cardiac center decreases heart rate
182
Q

chemoreceptors

A

•in aortic arch, carotid arteries and medulla oblongata
•sensitive to blood pH, CO2and O2levels
•more important in respiratory control than cardiac control
–if CO2accumulates in blood or CSF (hypercapnia), reacts with water and causes increase in H+levels
–H+lowers the pH of the blood possibly creating acidosis (pH < 7.35)
•hypercapnia and acidosis stimulate the cardiac center to increase heart rate
•also respond to hypoxemia –oxygen deficiency in the blood
–usually slows down the heart

183
Q

chemoreflexes and baroreflexes, responses to fluctuation in blood chemistry, are

A

both negative feedback loops

184
Q

Chronotropic Chemicals

A

chemicals affect heart rate as well as neurotransmitters from cardiac nerves
–blood-borne adrenal catecholamines (NE and epinephrine) are potent cardiac stimulants

185
Q

drugs that stimulate heart

A

–nicotine stimulates catecholamine secretion
–thyroid hormone increases number adrenergic receptors on heart so more responsive to sympathetic stimulation
–caffeine nhibits cAMP breakdown prolonging adrenergic effect

186
Q

electrolytes

A

–K+ has greatest chronotropic effect

–calcium

187
Q

hyperkalemia

A

excess K+diffuses into cardiocytes

–myocardium less excitable, heart rate slows and becomes irregular (inhibition of repolarization)

188
Q

hypokalemia

A

K+diffuses out of cardiocytes

–cells hyperpolarized, require increased stimulation

189
Q

hypercalcemia

A

excess of Ca2+

–decreases heart rate

190
Q

hypocalcemia

A

deficiency of Ca2+

–increases heart rate

191
Q

stroke volume

A

the other factor that in cardiac output, besides heart rate, is stroke volume

192
Q

three variables govern stroke volume:

A
  1. preload
  2. contractility
  3. afterload
193
Q

preload

A

the amount of tension in ventricular myocardium immediately before it begins to contract
–increased preload causes increased force of contraction
–exercise increases venous return and stretches myocardium
–cardiocytes generate more tension during contraction
–increased cardiac output matches increased venous return

194
Q

Frank-Sterling law of heart

A

SV inversely proportional to EDV
–stroke volume is proportional to the end diastolic volume
–ventricles eject as much blood as they receive
–the more they are stretched, the harder they contract

195
Q

contractility

A

refers to how hard the myocardium contracts for a given preload

196
Q

positive inotropic agents

A

increase contractility
–hypercalcemia can cause strong, prolonged contractions and even cardiac arrest in systole
–catecholamines increase calcium levels
–glucagon stimulates cAMP production
–digitalis raises intracellular calcium levels and contraction strength

197
Q

negative inotropic agents reduce contractility

A

–hypocalcemia can cause weak, irregular heartbeat and cardiac arrest in diastole
–hyperkalemiar educes strength of myocardial action potentials and the release of Ca2+ into the sarcoplasm
–vagus nerves have effect on atria but too few nerves to ventricles for a significant effect

198
Q

afterload

A

the blood pressure in the aorta and pulmonary trunk immediately distal to the semilunar valves
–opposes the opening of these valves
–limits stroke volume

199
Q

hypertension

A

increases afterload and opposes ventricular ejection

200
Q

anything that impedes arterial circulation can also increase afterload

A

–lung diseases that restrict pulmonary circulation

201
Q

cor pulmonale

A

right ventricular failure due to obstructed pulmonary circulation

202
Q

80Exercise and Cardiac Output

A

exercise makes the heart work harder and increases cardiac output

203
Q

exercise produces

A

ventricular hypertrophy
–increased stroke volume allows heart to beat more slowly at rest
–athletes with increased cardiac reserve can tolerate more exertion than a sedentary person

204
Q

coronary artery disease

A

(CAD) –a constriction of the coronary arteries
–usually the result of atherosclerosis–accumulation of lipid deposits that degrade the arterial wall and obstruct the lumen
–endothelium damaged by hypertension, virus, diabetes or other causes (e.g. free radicals!)
–monocytes penetrate walls of damaged vessels and transform into macrophages

205
Q

Effects of Atheromas

A

causes angina pectoris, intermittent chest pain, by obstructing 75% or more of the blood flow

206
Q

arteriosclerosis

A

hardened complicated plaque

207
Q

major risk factor for atherosclerosis is

A

excess of low-density lipoprotein (LDL) in the blood combined with defective LDL receptors in the arterial walls

208
Q

unavoidable risk factors

A

heredity, aging, being male

209
Q

avoidable risk factors

A

obesity, smoking, lack of exercise, anxious personality, stress, aggression, and diet

210
Q

coronary artery disease

treatment

A

–coronary bypass surgery
•great saphenous vein
–balloon angioplasty
–laser angioplasty

2 - Keiser A&P 2 (15 decks)

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