Cardiac physiology, Topnotch Flashcards

1
Q

Blood flow velocty in the aorta

A

11cm/sec

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2
Q

Blood flow velocity in the capillaries

A

0.03cm/sec

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3
Q

Control conduits for blood flow

A

Arterioles

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4
Q

Receptor for venous and arteriolar vasoconstriction in the skin, splanchnic, and renal circulation

A

a1

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5
Q

Receptor for arteriolar vasodilation in the skeletal muscles

A

b2

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6
Q

T/F: Capillaries undergo vasoconstriction and vasodilation

A

F

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7
Q

Law: Blood flow is proportional to pressure difference and inversely proportional to resistance

A

Ohm’s law

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8
Q

Law: Resistance is proportional to blood viscosity and length of vessel and inversely proportional to radius of vessel raised to the fourth power

A

Poiseuille’s law

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9
Q

Factors that affect Reynold’s number

A

1) Blood density
2) Blood viscosity
3) Blood flow velocity
4) Blood vessel diameter

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10
Q

Laminar vs turbulent: High Reynold’s number

A

Turbulent

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11
Q

Highest arterial BP

A

SBP

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12
Q

Lowest arterial BP

A

DBP

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13
Q

Systolic pressure-diastolic pressure

A

Pulse pressure

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14
Q

Central venous pressure is synonymous to ___ atrial pressure

A

Right

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15
Q

Pulmonary capillary wedge pressure estimates ___ atrial pressure

A

Left

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16
Q

Mean aortic pressure

A

100mmHg

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17
Q

Mean arteriolar pressure

A

50mmHg

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18
Q

Mean capillary pressure

A

20mmHg

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19
Q

Pressure in vena cava

A

4mmHg

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20
Q

Glomerular hydrostatic pressure

A

60mmHg

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21
Q

ECG: AV node conduction

A

PR segment

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22
Q

ECG: Conduction time through AV node

A

PR interval

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23
Q

ECG: Ventricular repolarization

A

T wave

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24
Q

ECG: Depolarization + repolarization of ventricles

A

QT interval

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25
Q

ECG: Plateau of ventricular action potential

A

ST segment

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26
Q

Effect on ECG: Flat/inverted T wave

A

Hypokalemia

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27
Q

Effect on ECG: Low P wave, tall T wave

A

Hyperkalemia

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28
Q

Effect on ECG: Prolonged QT interval

A

Hypocalcemia

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29
Q

Effect on ECG: Shortened QT interval

A

Hypercalcemia

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30
Q

PR segment

A

End of P wave, start of QRS complex

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31
Q

PR interval

A

Start of P wave, start of QRS complex

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32
Q

QT interval

A

Start of QRS complex, end of T wave

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33
Q

ST segment

A

End of QRS complex, start of T wave

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34
Q

Ventricular action potential: Phases

A

0-4

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35
Q

Ventricular action potential: Phase 0

A

Na influx (depolarization)

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36
Q

Ventricular action potential: Phase 1

A

K efflux (partial repolarization)

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37
Q

Ventricular action potential: Phase 2

A

Ca influx (plateau)

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38
Q

Ventricular action potential: Phase 3

A

K efflux (complete repolarization)

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39
Q

Ventricular action potential: Phase 4

A

RMP

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40
Q

SA node action potential: Phases

A

0,3,4

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41
Q

SA node action potential: Phase 0

A

Ca influx (depolarization)

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42
Q

SA node action potential: Phase 3

A

K efflux

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43
Q

SA node action potential: Phase 4

A

Slow Na influx towards threshold

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44
Q

Rate of phase 4 depolarization (fastest to slowest)

A

SA node > AV node > His-Purkinje system

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45
Q

Master pacemaker of the heart

A

SA node

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46
Q

Cardiac pacemaker with the slowest conduction velocity of 0.01-0.05m/sec

A

AV node

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47
Q

Cardiac pacemaker with the fastest conduction velocity of 2-4m/sec

A

His-Purkinje system

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48
Q

Intrinsic firing rate: SA node

A

70-80bpm

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49
Q

Intrinsic firing rate: AV node

A

40-60bpm

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50
Q

Intrinsic firing rate: Bundle of His

A

40bpm

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51
Q

Intrinsic firing rate: Purkinje fibers

A

15-20bpm

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52
Q

Stable vs unstable: RMP of SA node

A

Unstable

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53
Q

Stable vs unstable: RMP of latent pacemakers

A

Stable

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54
Q

RMP of latent pacemakers

A

-90mV

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55
Q

Time required for excitation to spread throughout cardiac tissue

A

Conduction velocity

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56
Q

Conduction velocity is proportional to

A

Inward current during upstroke

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57
Q

RMP of cardiac muscle is determined by

A

Conductance to K

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58
Q

Accounts for SA node automaticity

A

If/slow funny Na channels

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59
Q

Phase of cardiac AP responsible for setting the heart rate

A

Phase 4

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60
Q

Propagation of AP around the ventricles wherein the sign never reaches an area with ARP

A

Circus movements

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61
Q

Circus movements are the basis for

A

Vfib

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62
Q

Causes for circus movements (3)

A

1) Long conduction pathway
2) Decreased conduction velocity
3) Short refractory period

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63
Q

Condition wherein there is a long conduction pathway

A

Dilated cardiomyopathy

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64
Q

Conditions wherein there is decreased conduction velocity (3)

A

1) Ischemic heart
2) Hyperkalemia
3) Blocked Purkinje

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65
Q

Condition wherein there is a short refractory period

A

1) Epinephrine

2) Electrical stimulation

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66
Q

All Na inactivation gates closed

A

Absolute refractory period

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67
Q

Some Na inactivation gates start to open

A

Effective refractory period

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68
Q

T/F: AP can be conducted during ERP

A

F

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69
Q

AP can be conducted with a higher than normal stimulus

A

RRP

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70
Q

All Na inactivation gates open; membrane potential is higher than RMP

A

Supranormal period, cell is more excitable than normal

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71
Q

Drugs that change heart rate

A

Chronotropic

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72
Q

Drugs that change conduction velocity

A

Dromotropic

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73
Q

Drugs that change contractility

A

Inotropic

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74
Q

Drugs that change rate of relaxation

A

Lusitropic

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75
Q

Affected by chronotropes

A

SA node

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76
Q

Affected by dromotropes

A

AV node

77
Q

Affected by inotropes

A

Stroke volume

78
Q

Preload of the heart

A

Left ventricular end-diastolic volume

79
Q

Afterload of the heart

A

Aortic pressure

80
Q

Increase in preload will increase stroke volume within certain PHYSIOLOGIC LIMITS

A

Frank-Starling mechanism

81
Q

Frank-Starling mechanism is due to (2)

A

1) Maximum degree of overlap between actin and myosin

2) Reduction of space between thick and thin filaments

82
Q

Proportional vs inverse: LVEDV and venous return

A

Proportional

83
Q

Proportional vs inverse: LVEDV and right atrial pressure

A

Proportional

84
Q

Blood ejected by the ventricle per heart beat

A

Stroke volume

85
Q

Percentage of EDV ejected by the ventricle per heart beat

A

EF

86
Q

Total blood volume ejected per unit time

A

Cardiac output

87
Q

Formula: Stroke volume

A

EDV-ESV

88
Q

Formula: EF

A

SV/EDV

89
Q

Formula: CO

A

HR x SV

90
Q

Normal stroke volume

A

70mL

91
Q

Normal EF

A

55%

92
Q

Normal CO

A

5L/min

93
Q

Work the heart performs with each beat

A

Stroke work

94
Q

Work per unit time

A

Cardiac minute work

95
Q

Ratio of work output to total chemical energy expenditure

A

Maximum efficiency of cardiac contraction

96
Q

Stroke work is equal to

A

SV x aortic pressure

97
Q

Primary source of energy for stroke work

A

Fatty acids

98
Q

Cardiac minute work is equal to

A

CO x aortic pressure

99
Q

Myocardial O2 consumption is increased by (4)

A

1) Afterload
2) Size of heart
3) Contractility
4) Heart rate

100
Q

Normal maximum efficiency of cardiac contraction

A

20-25%

101
Q

Phases of the cardiac cycle

A

1) Atrial contraction/systole
2) Isovolumetric contraction
3) Rapid ventricular ejection
4) Slow ventricular ejection
5) Isovolumetric relaxation
6) Rapid ventricular filling
7) Slow ventricular filling

102
Q

Occurs during distal 3rd of systole

A

Atrial contraction

103
Q

T/F: Atrial contraction is essential for ventricular filling

A

F

104
Q

Atrial pressure wave seen with atrial contraction

A

a wave

105
Q

Abnormal heart sound heard with atrial contraction against a stiff ventricle

A

S4

106
Q

Atrial wave seen in isovolumetric contraction

A

c wave

107
Q

Heart sound heard during isovolumetric contraction

A

S1 (AV valves close)

108
Q

Atrial filling begins at this phase

A

Rapid ventricular ejection

109
Q

ECG wave seen in reduced ventricular ejection

A

T wave

110
Q

Phase of cardiac cycle where incisura of aortic pressure is seen

A

Isovolumetric relaxation

111
Q

Atrial pressure wave seen in isovolumetric relaxation

A

v wave

112
Q

Heart sound heard with isovolumetric relaxation

A

S2

113
Q

Heart sound heard during rapid ventricular filling

A

S3

114
Q

Rapid ventricular filling takes place in which part of diastole

A

First 1/3

115
Q

Longest phase of the cardiac cycle

A

Reduced ventricular filling

116
Q

Reduced ventricular filling is aka

A

Diastasis

117
Q

Length of reduced ventricular filling is dependent on

A

Heart rate

118
Q

Reduced ventricular filling occurs during

A

Middle 3rd of diastole

119
Q

Increase vs decrease in aortic pressure: Incisura

A

Increase

120
Q

BP control (3)

A

1) Central
2) Acute
3) Long-term

121
Q

Central control of heart rate and BP

A

Vasomotor area of medulla

122
Q

Portion of medulla: Excitatory to the CV system

A

Lateral

123
Q

Portion of medulla: Inhibitory to the CV system

A

Medial

124
Q

Acute controllers of BP

A

1) ANS
2) CNS ischemic response
3) Baroreceptors
4) Chemoreceptors
5) Lower pressure receptors

125
Q

Long-term control of BP

A

RAAS

126
Q

SY vs PSY: Greater control of the BP

A

SY

127
Q

Buffers minute-to-minute changes in BP

A

Baroreceptors

128
Q

Location of baroreceptors (2)

A

1) Carotid sinus

2) Aortic arch

129
Q

Carotid baroreceptors respond to increase/decrease in pressures from

A

50-180mmHg

130
Q

Aortic baroreceptors respond to pressure ___mmHg

A

> 80

131
Q

Chemoreceptors respond to (2)

A

1) Low O2
2) High CO2
3) GIVEN BP less than 80mmHg

132
Q

Location of low pressure receptors (2)

A

1) Atria

2) Pulmonary arteries

133
Q

Low pressure receptors respond to

A

Increased intravascular volume

134
Q

Responses of low pressure receptors

A

1) Increase ANP
2) Decrease ADH
3) Renal vasodilation
4) Increase heart rate

135
Q

Increase in heart rate to match vascular resistance with cardiac output

A

Brainbridge reflex

136
Q

CNS ischemic response starts at ___mmHg

A

Less than 60

137
Q

CNS ischemic response is optimal at ___mmHg

A

15-20

138
Q

In CNS ischemic response, all systemic arterioles vasoconstrict EXCEPT (2)

A

1) Cerebral vessels

2) Coronary vessels

139
Q

Cushing reflex/reaction is a response to

A

Increased ICP

140
Q

Cushing reflex/reaction: Triad

A

1) Htn
2) Bradycardia
3) Irregular respirations

141
Q

Responsible in maintaining normal BP despite wide variation in salt intake

A

RAAS

142
Q

RAAS takes ___ to take effect

A

20 minutes

143
Q

Normal capillary hydrostatic pressure

A

25mmHg

144
Q

Normal capillary oncotic pressure

A

28mmHg

145
Q

Normal interstitial hydrostatic pressure

A

-3mmHg

146
Q

Causes interstitial hydrostatic pressure to be negative

A

Lymphatic pump

147
Q

Normal interstitial oncotic pressure

A

8mmHg

148
Q

Hydraulic conductance of capillary wall

A

Filtration coefficient

149
Q

Normal net filtration in capillaries

A

2mL/min

150
Q

Net filtration pressure in kidneys

A

10mmHg

151
Q

Amount of lymph produced per day

A

2-3L

152
Q

T/F: Lymphatic vessels have valves

A

T

153
Q

Cause of edema in burns and inflammation

A

Increased filtration coefficient

154
Q

Mechanisms for control of local blood flow

A

1) Acute control

2) Long-term control

155
Q

Mechanisms for ACUTE control of LOCAL blood flow

A

1) Myogenic theory
2) Metabolic theory
3) Autoregulation

156
Q

Myogenic theory of BP control

A

Stretching of vascular smooth muscle causes a reflex contraction and vice verse

157
Q

Metabolic theory of BP control

A

Metabolic activity causes release of vasodilator substances

158
Q

Mechanisms under metabolic theory of BP control

A

1) O2/nutrient lack theory

2) Vasodilator theory

159
Q

O2 lack theory of BP control

A

O2 is needed for smooth muscle contraction and lack of O2 leads to vasodilation

160
Q

Nutrient lack theory of BP control

A

Thiamine, niacin, riboflavin, and glucose are needed for smooth muscle contraction and lack of these leads to vasodilation

161
Q

Vasodilator theory of BP control

A

Metabolism releases adenosine, CO2, K, and hydrogen, which are vasodilators

162
Q

Metabolic theory: Increase in blood flow in response to brief periods of decreased blood flow

A

Reactive hyperemia

163
Q

Metabolic theory: Increase in blood flow to meet increased metabolic demand

A

Active hyperemia

164
Q

Autoregulatory mechanism: Kidneys

A

Tubuloglomerular feedback

165
Q

Autoregulatory mechanism: Brain

A

Response to CO2 and H levels

166
Q

Autoregulatory mechanism: Heart

A

Response to perfusion pressure

167
Q

Mechanism for long-term control of LOCAL blood flow

A

Angiogenesis

168
Q

Susbtances that cause angiogenesis (3)

A

1) VEGF
2) FGF
3) Angiogenin

169
Q

Angiogenesis occurs in response to

A

Hypoxia

170
Q

Vascularity is determined by

A

MAXIMUM blood flow need

171
Q

Most potent vasoconstrictor

A

ET-1

172
Q

Vasodilator substance that counteracts TXA2

A

PGI2

173
Q

Vasodilator vs vasoconstrictor: NE

A

Vasoconstrictor

174
Q

Vasodilator vs vasoconstrictor: Epi

A

Vasoconstrictor

175
Q

Vasodilator vs vasoconstrictor: ANP

A

Vasodilator

176
Q

Vasodilator vs vasoconstrictor: H

A

Vasodilator

177
Q

Vasodilator vs vasoconstrictor: CO2

A

Vasodilator EXCEPT at pulmonary vascular bed

178
Q

Vasodilator vs vasoconstrictor: PGF

A

Vasoconstrictor

179
Q

Vasodilator vs vasoconstrictor: K

A

Vasodilator

180
Q

Vasodilator vs vasoconstrictor: TXA2

A

Vasoconstrictor

181
Q

Vasodilator vs vasoconstrictor: ATII

A

Vasoconstrictor

182
Q

Vasodilator vs vasoconstrictor: PGE

A

Vasodilator

183
Q

Vasodilator vs vasoconstrictor: Lactate

A

Vasodilator

184
Q

Vasodilator vs vasoconstrictor: Adenosine

A

Vasodilator

185
Q

Vasodilator vs vasoconstrictor: Bradykinin

A

Arteriolar vasodilator, venous vasoconstrictor

186
Q

Vasodilator vs vasoconstrictor: Histamine

A

Arteriolar vasodilator, venous vasoconstrictor

187
Q

Special circulation/s whose major metabolic control is local rather than central

A

1) Cerebral
2) Coronary
3) Pulmonary
4) Renal
5) Skeletal during exercise

188
Q

Special circulation/s whose major metabolic control is central (ANS) rather than local

A

Skin