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DMD 5247 > Heart Physiology- Winden > Flashcards

Heart Physiology- Winden Flashcards

1
Q

what is the valve between the right atrium and the right ventricle?

A

tricuspid

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2
Q

A red blood cell leaving the right lung would pass which structures (in order):

A

LA –> LV –>aorta/body–> RA

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3
Q

what is the prupose of the chordae tendineae?

A

helps keep the bi and tricuspid vavle from inverting

keeps blood flowing in one direction

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4
Q

Which chamber of the heart has the greatest volume?

A

The wall of the LV is larger bc pumps blood out to the body

the volume of the ventricles are the same

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5
Q

which is the bicuspid valve

A

between the LA and LV

(mitral, left AV valve)

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6
Q

When do I do CPR?

A

When someone’s heart has stopped

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7
Q

which of the following lines the chambers of the heart?

A

endocardium

(also line endothlium)

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8
Q

The right coronary artery arises from the anterior aortic sinus of the ascending aorta and runs forward between the pulmonary trunk and the right auricle.

The left coronary artery, which is usually longer than the right coronary artery, arises from the left posterior aortic sinus of the ascending aorta and passes forward between the pulmonary trunk and the left auricle.

A

both are true

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9
Q

All of the following carry deoxygenated blood from the systemic circuit and empty directly into the right atrium EXCEPT one. Which one is the EXCEPTION?

inferior vena cav

azygos vein

superior vena cava

coronary sinus

A

azygos vein

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10
Q

Which of the following valves guards the opening between the left atrium and left ventricle?

A

mitral valve

(bicuspid)

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11
Q

Which of the following structures prevents the AV valves from everting (or being blown out) back into the atria during ventricular contraction?

A

chordae tendineae and papillary muscle

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12
Q

The base of the heart is formed mainly by the

A

left atrium

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13
Q

Thrombosis in the coronary sinus might cause dilation of all of the following veins EXCEPT one.

great cardiac vein

middle cadiac vien

anterior cardiac vein

small cardiac vein

oblique cardiac vein

A

anterior cardiac vein

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14
Q

Which of the following describes the function of the ductus arteriosus in the fetus?

A

shunts blood from the pulmonary artery to the aorta

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15
Q

Inotropy

A

Force of contraction

positive inotropic

negative inotropic

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16
Q

chronotropy

A

rate of contractions

positive chronotropic

negative chronotropic

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17
Q

Dromotrophy

A

conduction velocity

postive dromotropic

negative dromotropic

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18
Q

Brady

A

slow

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19
Q

Tachy

A

fast

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20
Q

Tachycardia

A

fast beating heart

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21
Q

Bradycardia

A

slow beating heart

(below 70-100)

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22
Q

Arrhythmia

A

no rhythm

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23
Q

Dysrhythmia

A

irregular rhythm

atypical

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24
Q

Heartbeat

(series…)

A
  • A single contraction of the heart
  • entire heart contracts in series
    • First the atria
    • then the ventricles
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25
Q

two types of cardiac muscle cells

A

conducting system

contractile cells

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26
Q

conducting system

A

controls and coordinated heartbeat

myocytes

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27
Q

contractile cells

A

produce contractions that propel blood

myocyte

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28
Q

cardiac cycle starts with

A

action potential at SA node

  • transmitted through conducting system
  • produces action potentials in cardiac muscle cells (contractile cells)
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29
Q

Electrocardiogram (ECG or EKG)

A

electrical events in the cardiac cycle can be recorded on an electrocardiogram

measured AP

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30
Q

The conducting system

A

a system of specialized cardiac muscle cells

(initiates/distributes electrical impulses that stimulate contraction)

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31
Q

Automaticity

A

cardiac muscle tissue contracts automatically

(can go to thershold without additional stimulus)

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32
Q

Contractile Cells

A

Purkinje fibers distribute the stimulus to the contractile cells, which makes up most of the muscle cells in the heart

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33
Q

Resting potential

A

ventricular cell about 90 mV

Atrial cell about 80 mV

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34
Q

Conduction system ions

A

K+

Na +

Ca ++

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35
Q

Myocardium ions

A

K+

Na+

Ca++

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36
Q

Blood Vessels ions

A

Ca++

K+

Cl-

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37
Q

Action Potential in cariac muscle steps

A
  1. Rapid Depolarization
  2. Peak because of the K
  3. The plateau ( caused by Ca)
  4. Repolarization
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38
Q

absolute refractory period

A

the heart/ skeletal muscle cannot contract until the cycle is complete

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39
Q

Rapid Depolarization

A

cause: Na+ entry

duration: 3-5m sec

ends with: closure of voltage-gated fast sodium channels

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40
Q

The plateau

A

cause: Ca++

Duration: about 175 msec

Ends: closure of slow calcium channels

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41
Q

repolarization

A

cause: K+ loss

Duration: 75msec

ends with: closure of slow potassium channels

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42
Q

which only have an endothelial layer

A

capillaries

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43
Q

ventricles fill at about

A

70% before they contract

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44
Q

what take control of the heart,

A

SA node

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45
Q

Refractory Period

A

absolute refractory period

relative refractory period

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46
Q

absolute refractory period

A

long

cardiac muscle cells cannot respond

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47
Q

relative refractory period

A

short

response depends on degree of stimulus

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48
Q

timing of refractory periods

A
  • length of cardiac action potential in ventricular cell
  • 250-300 msec
    • 30 times longer than skeletal muscle fiber
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49
Q

Role of ca in skeletal muscle contraction

A
  1. Somatic motor neuron releases ACh at neuromuscular junction
  2. Net entry of Na+ through ACh receptor channel initiates a muscle action potiental
  3. AP in t tubule alters conformation of DHP receptor
  4. DHP receptor opens Ca2+ release channels in SR and Ca2+ enters cytoplasm
  5. Ca2+ binds to troponin allowing strong actin mysosin binding
  6. myosin heads execute power stroke
  7. actin filaments slides towards center of sarcomere
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50
Q

Smooth muscle

myocardium

skeletal muscle

Ca dependence

A

Smooth muscle: extraceullular ca

Myocardium: extracellular ca

skeletal muscle: intracellular ca

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51
Q

Ion channel drugs

A

Na+

Ca++

K+

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52
Q

Aerobic energy of heart

A
  • from mito breakdown of fatty acids and glucose
  • oxygen from circulating hemoglobin
  • cardiac muscle store oxygen in myoglobin
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53
Q

structures of conducting system

A
  • Sinoatrial (SA) node - wall of right atrium
  • Atrioventricular (AV) node - junction between atria and ventricles
  • Conducting cells - throughout myocardium
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54
Q

conducting cells

A

interconnect SA and AV nodes

distribute stimulates through myocardium

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55
Q

conducting in the atrium

A

internodal pathways

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56
Q

conducting cells in the ventricles

A

AV bundle and the bundle branches

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57
Q

Prepotential conducting cells

A
  • also called pacemker potential
  • resting potential (depolarizes toward threshold)
  • SA node depolarizes first, establishing heart rate

reaches potential thershold w/o any help.

Na leaks into cell via funny channels

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58
Q

SA node generates ______ action potentials per minute

A

80-100

parasympathetic stimulation slows heart rate

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59
Q

AV node generates _______ AP per minute

A

40-60

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60
Q

SA node

A

Sinoatrial Node

posterior wall of right atrium

contains pacemaker cells

connected to AV node by internodal pathways

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61
Q

the AV node is located in

A

floor of right atrium

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62
Q

what is the main parasympthaetic nerve ?

A

vegas

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63
Q

Ectopic pacemaker

A
  • Abnormal cells
  • Generate high rate of action potentials
  • Bypass conducting system
  • Disrupt ventricular contractions
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64
Q

The AV node is the pacemaker of the heart

the conducting system of the heart is all modiufies cardiac muscle fiber and not nerves

A

false (SA node), true

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65
Q

heart Impulse path

A

SA node–> atrial muscle–> av node–> bundle of his–> bundle branches–> purkinje fibers–> ventricular muscle

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66
Q

the presence fo the plateau in the AP causes causes ventricular contraction to lst as much as 15 times as long in cardiac muscle as in skeletal muscle

the strength of the cardiac muscle contraction is directly proportional to intracellular Na concentration

A

first is true

Second is false

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67
Q

craig has a tachycardia

A

sa node

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68
Q

if patient SA and AV nodes fail what happens?

A

both the atria and ventricles will contine to contract of set the pace of the buncle of His (30-40 impulses per minute)

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69
Q

ECG or EKG

A

Electrocardiogram

  • a recording of electrical events in the heart
  • obtained by electrodes at specific body locatoins
  • abnormal patterens diagnose damage
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70
Q

do we have electrical impulses in the heart?

A

yes, due to ion channels

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71
Q

P wave

A

atria depolarize

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72
Q

QRS complex

A

ventricles depolarize

ventricles contractions

(larger than p wave beacuse ventrical has more muscle than the atrium)

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73
Q

T wave

A

ventricles repolarize

ventrial relaxation

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74
Q

P-R interval

A

from start of atrial depolarization

to start of QRS complex

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75
Q

Q-T interval

A

from ventricular depolarization

to ventricular repolarization

76
Q

which poriton of the ECG is the only isoelctrical period when the entire ventricle is depolarized

A

S-T segment

77
Q

this portion of the ecg reps ventricular repolarization

A

T wave

78
Q

this portion of the ECG ___

A

S-T segment

79
Q

electrocardiograph is a rep. of what?

A

cardiac conductuion sytstem

80
Q

long refreactory period prevents

A

summations and tetany

81
Q

contraction of a cardiac muscle cell produced by an increase in

A

Ca ion concentrations

82
Q

role of calcium ions in cardiac contractions

A
  • 20% of Ca ions required for a contraction of extraceullar
83
Q

calcium ions enter plasma membrane during

A

plateau phase

84
Q

arrival of extraceullar Ca 2+ triggers release of

A

calcium ion reserves from sacroplasmic reticulum

85
Q

As slow calcium channels close

A

INtracellular Ca is absobed by the SR or pump out of the cell

86
Q

cardiac muscle tissue is very sensitive to extracellular

A

ca concentrations

87
Q

AV bundle

A

in septum

carris impulse to left and right bundle branches (–> Purkinje fibers)

then to moderator band (–>papillary muscles)

88
Q

Purkinje fibers

A

distribute impulse through ventricles

atrial contraction is completed

ventricular contraction starts

89
Q

what are the differnt portions of the ECG

A
90
Q

Premature atrial contractions

A

another P wave (premature atrial contractions)

91
Q

Proxysmal Atrial tachycardia

A

PAT

atria are happening to quickly, ventricles are following

92
Q

Atrial FIbrillation (AF)

A

no p wave, atria are not defined (no coordinated top down contraciton)

ventricles are working bc av nodes allows ventricles to contract

93
Q

Premature ventricular contractions (PVCs)

A

extra beat, ventricle kicked in early

94
Q

Ventricle tachycardia

A

only QRS wave

ventricular

95
Q

Ventricular Fibrillation (VF)

A

no corrdinated contraction

no blood circulating

96
Q

the cardiac cycle

A

period between the start of one heartbeat and the beginning of the next

includes both contraction and relaxation

97
Q

the two phases of the cardiac cycle

A

systole (contraction)

diastole (relaxation)

98
Q

The four phases of the cardiac cycle

A

Atrial systole
Atrial diastole
Ventricular systole
Ventricular diastole

99
Q

atrial systole

A

Atrial contraction begins
Right and left AV valves are open

100
Q

Atria eject blood into ventricles

A

filling ventricles

101
Q

Atrial systole ends

A

AV valves close
Ventricles contain maximum blood volume
Known as end-diastolic volume (EDV)

102
Q

ventricles contract and build pressure

A

AV valves close cause isovolumetric contraction

103
Q

Ventricular ejection

A
  • Ventricular pressure exceeds vessel pressure
  • opening the semilunar valves and allowing blood to leave the ventricle
  • Amount of blood ejected is called the stroke volume (SV)
104
Q

Ventricular pressure falls

A

semilunar valves close

Ventricles contain end-systolic volume (ESV), about 40% of end-diastolic volume

105
Q

End- systolic volume (ESV)

A

about 40% of end diastolic volume

106
Q

Ventricles contract and build pressure

A

AV valves close cause isovolumetric contraction

107
Q

Ventricular ejection

A

  • Ventricular pressure exceeds vessel pressure opening the semilunar valves and allowing blood to leave the ventricle
  • Amount of blood ejected is called the stroke volume (SV)
108
Q

amount of blood ejected is called

A

Ventricular ejection

stroke volume (SV)

109
Q

Ventricular diastole

A

Ventricular pressure is higher than atrial pressure
All heart valves are closed
Ventricles relax (isovolumetric relaxation)

110
Q

another name for ventricular diastole/ relaxation

A

isovolumetric relaxation

111
Q

Atrail pressure is higher than ventricular pressure

A

AV valves open

passive atrial filling

passive ventricular filling

112
Q

blood pressure in any chamber

A

rise during systole

falls during diastole

113
Q

blood flows from _______ to ______.

controlled by

A

high to low pressure

controlled By:

  • timing of contractions
  • one-way valves
114
Q

At 75 beats per minute the cardiac cycle lasts about

A

800 msec

115
Q

when heart rate increases what hapen to the cardiac cycle?

A

all phases of cardiac cycle shorten

**mainly diastole

116
Q

Heart sound 1

A

Lound souns

produced by AV valves

117
Q

Heart sound 2

A

loud sounds

produced by semilunar valves

118
Q

Heart sounds 3 and 4

A

soft sounds

blood flow into ventricles and atrial contraction

119
Q

heart murmur

A

sounds produced by reguritation thorugh valves

120
Q

Cardiodynamics

A

the movements and force generatd by cardiac contractions

121
Q

How to calulate SV

A

SV= EDV-ESV

EDV- end-diastolic volume

ESV-End-systolic volume

122
Q

ejection fraction

A

the percentage of EDV represented by Stroke Volume

123
Q

what is cardiac output

A

Co

the volume pumped by left ventricle in 1 minute

124
Q

how to calculate cardiac output

A

CO= HR x SV

CO = cardiac output (mL/min)
HR = heart rate (beats/min)
SV = stroke volume (mL/beat)
125
Q

cardiac output adjusted by

A

changes in the heart rate or stroke volume

126
Q

heart rate is adujusted by

A

autonomic nervous system or hormones

127
Q

stroke volum adjusted by

A

changing EDV or ESV

128
Q

factors that affect heart rate (HR)

A

autonomic innervation

hormones

129
Q

factors affecting stroke volume

A

end diastolic volume

end systolic volume

130
Q

what affects cardiac output?

A

heart rate

and stroke volume

131
Q

Autonomic innercation of heart (3)

A

cardiac plexuses

vagus nerves (N X)

cardiac centers in medulla oblongata

132
Q

what innervate the heart

A

cardiac plexuses

133
Q

vagus nerves carry

A

parasympathetic preganglionic fibers to small ganglia in cardiac plexus

134
Q

cardiac centers of medulla oblongata

A

cardioacceleratory center

cardioinhibitory center

135
Q

cardioacceleratory center

A

controls sympathetic neurons

(increases heart rate)

136
Q

cardioinhibitory center of medulla oblongata

A

controls parasmpathetic neurons (slows heart rate)

137
Q

cardiac cholinergic receptors

A

activated by parasympathetic

M2 muscarinic receptors: mainly in SA Node

M2 activation: Reduces heart rate (negative chronotropic)

138
Q

Adrenergic heart receptors

A

activated by sympathetic

β1 Angioadrenergic receptors in myocardium, SA Node
β1 activation: Increases contractility (positive inotropic)
:Increases heart rate (positive chronotropic)

139
Q

Angiotensin

A

AT1 Myocardium: positive inotropy

140
Q

cardiac centers monitor

A 
Blood pressure (baroreceptors)
Arterial oxygen and carbon dioxide levels (chemoreceptors
141
Q

cardiac centers adjust

A

cardiac activity

142
Q

Autonomic tone:

A
  • Dual innervation maintains resting tone by releasing ACh and NE
143
Q

effects of the SA node

A
  • membrane potential of pacemaker cells
  • Rate of spontaneous depolarization depends on
144
Q

membrane potential of pacemaker cells

A

lower thatn other cardiac cells

145
Q

rate of spontaneous depolarization depends on

A

resting membrane potential

rate of depolarization

146
Q

pacemaker cells have membrane potentials closer to

A

threshold than those of other rcardiac muscle cells

(-60 mV vs -90mV)

147
Q

effects on the SA node

sympathetic and parasympathetic stimulation

A

greatest at SA node (heart rate)

148
Q

effects of SA node

ACh

A

parasympathetic stimulation

slows the heart

149
Q

effects on the SA node NE

A

sympathetic stimulation

speeds the heart

150
Q

parasympathetic stimulation releases

A

Ach

which extends repolarization and dcreases the rate of spontaneous depolarization

(heart rate slows)

151
Q

Brainbridge reflex

A

atrial reflex

adjusts heart rate in response to venous return

152
Q

strech receptors in right atrium

A

trigger increase in heart rate through increased sympathetic activity

153
Q

hormonal effects on heart rate

A

increase heart rate (by sympathetic stimulation of SA node)

154
Q

which hormones effect the heart rate

A

Epinephrine E

Norepinephrine (NE)

thyroid hormone

155
Q

Depolarization of the ventricles is represented on an electrocardiogram by the

A

QRS complex

156
Q

the normal pacemaker of the heart is

A

Sinoatrial node

157
Q

Factors affecting the stroke volume

A

filling time: duration of ventrical diastole

Venous return: rate of blood flow during ventrical diastole

158
Q

three factors that affect ESV

A

preload

contractility

afterload

159
Q

preload

A

ventricular stretching during diastole

proportional to EDV

affects ability of muscle cells to produce tension)

160
Q

contractility

A

force produced diring contraction at a given preload

161
Q

afterload

A

tension the ventricle produces to open the semilunar valve and eject blood

162
Q

The EDV and stroke volume at rest

A

EDV is low

Myocardium stretches less

stroke volume is low

163
Q

EDV and stroke volume with exercise

A

EDV increases

myocardium streches more

stroke volume increases

164
Q

frank-starling principle

A

as EDV increases, stroke colume increases

165
Q

Ventricular expansion limited by

A

Myocardial connective tissue

the cardiac(fibrous) skeleton

the pericardial sac

166
Q

more blood in ventricle means

A

> more forceful contraction

167
Q

frank-starling law of contraction

A

The force of contraction of myocardium is directly proportional to the stretch of the muscle (preload)

helps to pump out the blood received by the heart without excessive accumulation

168
Q

End- systolic volume (ESV)

A

amount of blood that remains in the ventricle at the end of ventricular systole

169
Q

contractility is affected by

A

autonomic activity

hormones

170
Q

Effects of Autonomic Activity on Contractility
Sympathetic stimulation

A
  • NE released by postganglionic fibers of cardiac nerves
  • Epinephrine and NE released by adrenal medullae
  • Causes ventricles to contract with more force
171
Q

Effects of Autonomic Activity on Contractility
Parasympathetic activity

A

Acetylcholine released by vagus nerves
Reduces force of cardiac contractions

172
Q

as afterload increases stroke volume

A

decreases

173
Q

heart rate control factors

A
  • autonomic nervous system (sympathetic and parasympathetic)
  • Circulating hormones
  • Venous return and stretch receptors
174
Q

EDV

stroke volume control

A

filling time and rate of venous return

175
Q

ESV

stroke volume control factors

A

preload, contractility, afterload

176
Q

on the surface of the chest, the apex of the heart is located:

A

in the left fifth intercostal space

177
Q

the dub is the sound of which valve

A

aortic and pulmonary

178
Q

tricuspid valve is located between which two chambers of the heart?

which valve has a unquie

A

right A and V

mitral

179
Q

where should you put the stethoscope to listen to the sound of the tricuspid valve

A

right half of the lower end of the body of the sternum

180
Q
A

A) Semilunar valve opens

181
Q

Tetanic muscle contractions don’t occur in a normal cardiac muscle because

A

the refractory period lasts until the muscle relaxes

182
Q

The phase in the cardiac cycle when the mitral valve is closed and the aortic valve is open is the

A

systolic ejection phase

183
Q

what is the parasympathetic nerve for the heart?

A

vegas nerve

184
Q

Resistance=

A

viscosity(of blood) x length of vessel

radius^4

185
Q

flow=

A

flow=( intial pressure-final pressure)/resistance

DMD 5247 (7 decks)

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