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Flashcards in 0-1 Chapter 19 the heart Deck (210):
1

cardiology

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

2

cardiovascular system

heart and blood vessels

3

circulatory system

heart, blood vessels, and the blood

4

major divisions of circulatory system

pulmonary circuit
systemic circuit

5

pulmonary circuit

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

6

systemic circuit

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

7

Heart

heart located in mediastinum, between lungs
tilted to the left

8

base

wide, superior portion of heart, blood vessels attach here

9

apex

inferior end, tilts to the left, tapers to point

10

pericardium

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

11

parietal pericardium

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

12

visceral pericardium

(epicardium) –heart covering
–serous lining of sac turns inward at base of heart to cover the heart surface

13

pericardial cavity

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

14

pericarditis

inflammation of the membranes
–painful friction rub with each heartbeat

15

epicardium

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

16

endocardium

–smooth inner lining of heart and blood vessels
–covers the valve surfaces and continuous with endothelium of blood vessels

17

myocardium

layer of cardiac muscle proportional to work load
•muscle spirals around heart which produces wringing motion

18

fibrous skeleton of the heart

-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

19

four chambers

right and left atria
right and left ventricles

20

right and left atria

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

21

right and left ventricles

two inferior chambers
•pump blood into arteries

22

atrioventricular sulcus

-separates atria and ventricles
-sulci contain coronary arteries

23

interventricular sulcus

-overlies the interventricular septum that divides the right ventricle from the left
-sulci contain coronary arteries

24

interatrial septum

–wall that separates atria

25

pectinate muscles

internal ridges of myocardium in right atrium

26

interventricular septum

muscular wall that separates ventricles

27

trabeculae carneae

internal ridges in both ventricles

28

Heart Valves

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

29

atrioventricular (AV) valves

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)

30

chordae tendineae

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

31

tricuspid valve

right AV valve has 3 cusps (tricuspid valve)

32

bicuspid valve

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

33

semilunar valves

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

34

pulmonary semilunar valve

in opening between right ventricle and pulmonary trunk

35

aortic semilunar valve

in opening between left ventricle and aorta

36

AV Valve Mechanics

ventricles relax

–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

37

AV Valve Mechanics

ventricles contract

–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

38

Blood Flow Through Heart

part 1

-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.

39

Blood Flow Through Heart

part 2

-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

40

Coronary Circulation

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

41

left coronary artery

(LCA) branch off the ascending aorta
-anterior interventricular branch
-circumflex branch

42

anterior interventricular branch

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

43

circumflex branch

•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

44

right coronary artery

RCA) branch off the ascending aorta
–supplies right atrium and sinoatrial node (pacemaker)

45

right marginal branch

•supplies lateral aspect of right atrium and ventricle

46

posterior interventricular branch

supplies posterior walls of ventricles

47

myocardial infarction

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

48

blood flow to the heart muscle during ventricular contraction is

slowed, unlike the rest of the body

49

three reasons:

–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

50

angina pectoris

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

51

myocardial infarction

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

52

Venous Drainage of Heart

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

53

the rest returns to right atrium by the following routes:

great cardiac vein
middle cardiac vein
left marginal vein

54

great cardiac vein

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

55

middle cardiac vein

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

56

left marginal vein

•empties into coronary sinus

57

coronary sinus

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

58

cardiocytes

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

59

intercalated discs

join cardiocytes end to end

60

interdigitating folds

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

61

mechanical junctions

tightly join cardiocytes

62

fascia adherens

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

63

desmosomes

weldlike mechanical junctions between cells
–prevents cardiocytes from being pulled apart

64

electrical junctions

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

65

repair of damage of cardiac muscle is almost entirely by

fibrosis (scarring)

66

cardiac muscle depends almost exclusively on

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

67

adaptable to organic fuels used

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

68

fatigue resistant

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

69

Cardiac Conduction System

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

70

Cardiac Conduction System

Order

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

71

sinoatrial (SA) node

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

72

atrioventricular (AV) node

–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

73

atrioventricular (AV) bundle (bundle of His)

–bundle forks into right and left bundle branches
–these branches pass through interventricular septum toward apex

74

Purkinje fibers

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

75

Cardiac Conduction System

sequence

-SA node fires
-Excitation spreads through atrial myocardium
-.AV node fires
-Excitation spreads down AV bundle
-Purkinje fibers distribute excitation through ventricular myocardium.

76

sympathetic nerves

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

77

sympathetic nerves

path

–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

78

parasympathetic nerves

(slows heart rate)
•parasympathetic stimulation reduces the heart rate

79

parasympathetic nerves


path


–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

80

systole

atrial or ventricular contraction

81

diastole

atrial or ventricular relaxation

82

sinus rhythm

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)

83

ectopic focus

another parts of heart fires before SA node
–caused by hypoxia, electrolyte imbalance, or caffeine, nicotine, and other drugs

84

Abnormal Heart Rhythms

spontaneous firing from some part of heart not the SA node

85

ectopic foci

region of spontaneous firing

86

nodal rhythm

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

87

intrinsic ventricular rhythm

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

88

arrhythmia

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

89

Cardiac Arrhythmias

atrial flutter
premature ventricular contractions
ventricular fibrillation

90

atrial flutter

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

91

premature ventricular contractions

–caused by stimulants, stress or lack of sleep

92

ventricular fibrillation

–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

defibrillation

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

94

SA node

•SA node is the system‟s pacemaker

95

SA node does not have a stable resting membrane potential

–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

each depolarization of the SA node sets off one heartbeat

one heartbeat
-at rest, fires every 0.8 seconds or 75 bpm

97

Impulse Conduction to Myocardium

•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

Electrical Behavior of Myocardium

•cardiocytes have a stable resting potential of -90 mV
•depolarize only when stimulated

99

depolarization phase

(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

plateau phase

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

repolarization phase

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

102

has a long absolute refractory period of

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

Action Potential of a Cardiocyte

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

Electrocardiogram

(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

ECG Deflections

P wave
QRS complex
ST segment -ventricular systole
T wave

106

P wave

–SA node fires, atria depolarize and contract
–atrial systole begins 100 msec after SA signal

107

QRS complex

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

108

ST segment -ventricular systole

–plateau in myocardial action potential

109

T wave

–ventricular repolarization and relaxation

110

Electrical Activity of Myocardium

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

Diagnostic Value of ECG

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

112

cardiac cycle

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

113

atrial systole

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

114

atrial diastole

occurs while ventricles in systole

115

quiescent period

all four chambers relaxed at same time

116

two main variables that govern fluid movement:

pressure
resistance

117

pressure

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

118

resistance

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

119

Pressure Gradients and Flow

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

events occurring on left side of heart

–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

opening and closing of valves are governed

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

122

valvular insufficiency

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

123

valvular stenosis

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

heart murmur

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

125

mitral valve prolapse

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

auscultation

listening to sounds made by body

127

first heart sound

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

128

second heart sound

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

129

Phases of Cardiac Cycle

•ventricular filling
•isovolumetric contraction
•ventricular ejection
•isovolumetric relaxation

130

Ventricular Filling

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

131

ventricular filling occurs in three phases:

rapid ventricular filling
diastasis
atrial systole

132

rapid ventricular filling

first one-third
•blood enters very quickly

133

diastasis

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

134

atrial systole

final one-third
•atria contract

135

end-diastolic volume

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

136

Isovolumetric Contraction

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

137

atria repolarize and relax

–remain in diastole for the rest of the cardiac cycle

138

ventricles depolarize

create the QRS complex, and begin to contract

139

AV valves close

as ventricular blood surges back against the cusps

140

heart sound S1

occurs at the beginning of this phase

141

isovolumetric‟

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

cardiocytes exert force, but

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

143

Ventricular Ejection

•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

rapid ejection

blood spurts out of each ventricle rapidly at first

145

reduced ejection

then more slowly under reduced pressure

146

ventricular ejections last

about 200 –250 msec
–corresponds to the plateau phase of the cardiac action potential

147

T wave occurs

late in this phase

148

stroke volume (SV)

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

149

ejection fraction

of about 54%
–as high as 90% in vigorous exercise

150

end-systolic volume (ESV

the 60 mL of blood left behind

151

Isovolumetric Relaxation

early ventricular diastole
–when T wave ends and the ventricles begin to expand

152

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

–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

when AV valves open

ventricular filling begins again

154

Timing of Cardiac Cycle

in a resting person

–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

total duration of the cardiac cycle is

therefore 0.8 sec in a heart beating 75 bpm

156

Overview of Volume Changes

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

Unbalanced Ventricular Output

pulmonary edema

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

158

Unbalanced Ventricular Output

peripheral edema

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

159

congestive heart failure

(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

left ventricular failure

blood backs up into the lungs causing pulmonary edema
–shortness of breath or sense of suffocation

161

right ventricular failure

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

cardiac output

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

163

cardiac output =

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

cardiac reserve

the difference between a person‟s maximum and resting CO
–increases with fitness, decreases with disease

165

pulse

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

166

pulse rates

–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

tachycardia

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

168

bradycardia

resting adult heart rate of less than 60 bpm
–in sleep, low body temperature, and endurance trained athletes

169

positive chronotropic agents

factors that raise the heart rate

170

negative chronotropic agents

factors that lower heart rate

171

Chronotropic Effects of the Autonomic Nervous System

•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

cardiostimulatory effect

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

173

cardioinhibitory effect

others transmit parasympathetic signals by way of the vagus nerve

174

sympathetic postganglionic fibers are adrenergic

–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

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

–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

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

of 100 bpm

177

vagal tone

holds down this heart rate to 70 –80 bpm at rest
–steady background firing rate of the vagus nerves

178

cardiac centers in the medulla

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

179

higher brain centers

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

180

proprioceptors in the muscles and joints

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

181

baroreceptors signal cardiac center

•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

chemoreceptors

•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

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

both negative feedback loops

184

Chronotropic Chemicals

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

185

drugs that stimulate heart

–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

electrolytes

–K+ has greatest chronotropic effect
–calcium

187

hyperkalemia

excess K+diffuses into cardiocytes
–myocardium less excitable, heart rate slows and becomes irregular (inhibition of repolarization)

188

hypokalemia

K+diffuses out of cardiocytes
–cells hyperpolarized, require increased stimulation

189

hypercalcemia

excess of Ca2+
–decreases heart rate

190

hypocalcemia

deficiency of Ca2+
–increases heart rate

191

stroke volume

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

192

three variables govern stroke volume:

1.preload
2.contractility
3.afterload

193

preload

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

Frank-Sterling law of heart

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

contractility

refers to how hard the myocardium contracts for a given preload

196

positive inotropic agents

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

negative inotropic agents reduce contractility

–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

afterload

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

hypertension

increases afterload and opposes ventricular ejection

200

anything that impedes arterial circulation can also increase afterload

–lung diseases that restrict pulmonary circulation

201

cor pulmonale

right ventricular failure due to obstructed pulmonary circulation

202

80Exercise and Cardiac Output

exercise makes the heart work harder and increases cardiac output

203

exercise produces

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

coronary artery disease

(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

Effects of Atheromas

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

206

arteriosclerosis

hardened complicated plaque

207

major risk factor for atherosclerosis is

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

208

unavoidable risk factors

heredity, aging, being male

209

avoidable risk factors

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

210

coronary artery disease

treatment

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