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Flashcards in Cardiac physiology, Topnotch Deck (188):
1

Blood flow velocty in the aorta

11cm/sec

2

Blood flow velocity in the capillaries

0.03cm/sec

3

Control conduits for blood flow

Arterioles

4

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

a1

5

Receptor for arteriolar vasodilation in the skeletal muscles

b2

6

T/F: Capillaries undergo vasoconstriction and vasodilation

F

7

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

Ohm's law

8

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

Poiseuille's law

9

Factors that affect Reynold's number

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

10

Laminar vs turbulent: High Reynold's number

Turbulent

11

Highest arterial BP

SBP

12

Lowest arterial BP

DBP

13

Systolic pressure-diastolic pressure

Pulse pressure

14

Central venous pressure is synonymous to ___ atrial pressure

Right

15

Pulmonary capillary wedge pressure estimates ___ atrial pressure

Left

16

Mean aortic pressure

100mmHg

17

Mean arteriolar pressure

50mmHg

18

Mean capillary pressure

20mmHg

19

Pressure in vena cava

4mmHg

20

Glomerular hydrostatic pressure

60mmHg

21

ECG: AV node conduction

PR segment

22

ECG: Conduction time through AV node

PR interval

23

ECG: Ventricular repolarization

T wave

24

ECG: Depolarization + repolarization of ventricles

QT interval

25

ECG: Plateau of ventricular action potential

ST segment

26

Effect on ECG: Flat/inverted T wave

Hypokalemia

27

Effect on ECG: Low P wave, tall T wave

Hyperkalemia

28

Effect on ECG: Prolonged QT interval

Hypocalcemia

29

Effect on ECG: Shortened QT interval

Hypercalcemia

30

PR segment

End of P wave, start of QRS complex

31

PR interval

Start of P wave, start of QRS complex

32

QT interval

Start of QRS complex, end of T wave

33

ST segment

End of QRS complex, start of T wave

34

Ventricular action potential: Phases

0-4

35

Ventricular action potential: Phase 0

Na influx (depolarization)

36

Ventricular action potential: Phase 1

K efflux (partial repolarization)

37

Ventricular action potential: Phase 2

Ca influx (plateau)

38

Ventricular action potential: Phase 3

K efflux (complete repolarization)

39

Ventricular action potential: Phase 4

RMP

40

SA node action potential: Phases

0,3,4

41

SA node action potential: Phase 0

Ca influx (depolarization)

42

SA node action potential: Phase 3

K efflux

43

SA node action potential: Phase 4

Slow Na influx towards threshold

44

Rate of phase 4 depolarization (fastest to slowest)

SA node > AV node > His-Purkinje system

45

Master pacemaker of the heart

SA node

46

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

AV node

47

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

His-Purkinje system

48

Intrinsic firing rate: SA node

70-80bpm

49

Intrinsic firing rate: AV node

40-60bpm

50

Intrinsic firing rate: Bundle of His

40bpm

51

Intrinsic firing rate: Purkinje fibers

15-20bpm

52

Stable vs unstable: RMP of SA node

Unstable

53

Stable vs unstable: RMP of latent pacemakers

Stable

54

RMP of latent pacemakers

-90mV

55

Time required for excitation to spread throughout cardiac tissue

Conduction velocity

56

Conduction velocity is proportional to

Inward current during upstroke

57

RMP of cardiac muscle is determined by

Conductance to K

58

Accounts for SA node automaticity

If/slow funny Na channels

59

Phase of cardiac AP responsible for setting the heart rate

Phase 4

60

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

Circus movements

61

Circus movements are the basis for

Vfib

62

Causes for circus movements (3)

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

63

Condition wherein there is a long conduction pathway

Dilated cardiomyopathy

64

Conditions wherein there is decreased conduction velocity (3)

1) Ischemic heart
2) Hyperkalemia
3) Blocked Purkinje

65

Condition wherein there is a short refractory period

1) Epinephrine
2) Electrical stimulation

66

All Na inactivation gates closed

Absolute refractory period

67

Some Na inactivation gates start to open

Effective refractory period

68

T/F: AP can be conducted during ERP

F

69

AP can be conducted with a higher than normal stimulus

RRP

70

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

Supranormal period, cell is more excitable than normal

71

Drugs that change heart rate

Chronotropic

72

Drugs that change conduction velocity

Dromotropic

73

Drugs that change contractility

Inotropic

74

Drugs that change rate of relaxation

Lusitropic

75

Affected by chronotropes

SA node

76

Affected by dromotropes

AV node

77

Affected by inotropes

Stroke volume

78

Preload of the heart

Left ventricular end-diastolic volume

79

Afterload of the heart

Aortic pressure

80

Increase in preload will increase stroke volume within certain PHYSIOLOGIC LIMITS

Frank-Starling mechanism

81

Frank-Starling mechanism is due to (2)

1) Maximum degree of overlap between actin and myosin
2) Reduction of space between thick and thin filaments

82

Proportional vs inverse: LVEDV and venous return

Proportional

83

Proportional vs inverse: LVEDV and right atrial pressure

Proportional

84

Blood ejected by the ventricle per heart beat

Stroke volume

85

Percentage of EDV ejected by the ventricle per heart beat

EF

86

Total blood volume ejected per unit time

Cardiac output

87

Formula: Stroke volume

EDV-ESV

88

Formula: EF

SV/EDV

89

Formula: CO

HR x SV

90

Normal stroke volume

70mL

91

Normal EF

55%

92

Normal CO

5L/min

93

Work the heart performs with each beat

Stroke work

94

Work per unit time

Cardiac minute work

95

Ratio of work output to total chemical energy expenditure

Maximum efficiency of cardiac contraction

96

Stroke work is equal to

SV x aortic pressure

97

Primary source of energy for stroke work

Fatty acids

98

Cardiac minute work is equal to

CO x aortic pressure

99

Myocardial O2 consumption is increased by (4)

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

100

Normal maximum efficiency of cardiac contraction

20-25%

101

Phases of the cardiac cycle

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

Occurs during distal 3rd of systole

Atrial contraction

103

T/F: Atrial contraction is essential for ventricular filling

F

104

Atrial pressure wave seen with atrial contraction

a wave

105

Abnormal heart sound heard with atrial contraction against a stiff ventricle

S4

106

Atrial wave seen in isovolumetric contraction

c wave

107

Heart sound heard during isovolumetric contraction

S1 (AV valves close)

108

Atrial filling begins at this phase

Rapid ventricular ejection

109

ECG wave seen in reduced ventricular ejection

T wave

110

Phase of cardiac cycle where incisura of aortic pressure is seen

Isovolumetric relaxation

111

Atrial pressure wave seen in isovolumetric relaxation

v wave

112

Heart sound heard with isovolumetric relaxation

S2

113

Heart sound heard during rapid ventricular filling

S3

114

Rapid ventricular filling takes place in which part of diastole

First 1/3

115

Longest phase of the cardiac cycle

Reduced ventricular filling

116

Reduced ventricular filling is aka

Diastasis

117

Length of reduced ventricular filling is dependent on

Heart rate

118

Reduced ventricular filling occurs during

Middle 3rd of diastole

119

Increase vs decrease in aortic pressure: Incisura

Increase

120

BP control (3)

1) Central
2) Acute
3) Long-term

121

Central control of heart rate and BP

Vasomotor area of medulla

122

Portion of medulla: Excitatory to the CV system

Lateral

123

Portion of medulla: Inhibitory to the CV system

Medial

124

Acute controllers of BP

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

125

Long-term control of BP

RAAS

126

SY vs PSY: Greater control of the BP

SY

127

Buffers minute-to-minute changes in BP

Baroreceptors

128

Location of baroreceptors (2)

1) Carotid sinus
2) Aortic arch

129

Carotid baroreceptors respond to increase/decrease in pressures from

50-180mmHg

130

Aortic baroreceptors respond to pressure ___mmHg

>80

131

Chemoreceptors respond to (2)

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

132

Location of low pressure receptors (2)

1) Atria
2) Pulmonary arteries

133

Low pressure receptors respond to

Increased intravascular volume

134

Responses of low pressure receptors

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

135

Increase in heart rate to match vascular resistance with cardiac output

Brainbridge reflex

136

CNS ischemic response starts at ___mmHg

Less than 60

137

CNS ischemic response is optimal at ___mmHg

15-20

138

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

1) Cerebral vessels
2) Coronary vessels

139

Cushing reflex/reaction is a response to

Increased ICP

140

Cushing reflex/reaction: Triad

1) Htn
2) Bradycardia
3) Irregular respirations

141

Responsible in maintaining normal BP despite wide variation in salt intake

RAAS

142

RAAS takes ___ to take effect

20 minutes

143

Normal capillary hydrostatic pressure

25mmHg

144

Normal capillary oncotic pressure

28mmHg

145

Normal interstitial hydrostatic pressure

-3mmHg

146

Causes interstitial hydrostatic pressure to be negative

Lymphatic pump

147

Normal interstitial oncotic pressure

8mmHg

148

Hydraulic conductance of capillary wall

Filtration coefficient

149

Normal net filtration in capillaries

2mL/min

150

Net filtration pressure in kidneys

10mmHg

151

Amount of lymph produced per day

2-3L

152

T/F: Lymphatic vessels have valves

T

153

Cause of edema in burns and inflammation

Increased filtration coefficient

154

Mechanisms for control of local blood flow

1) Acute control
2) Long-term control

155

Mechanisms for ACUTE control of LOCAL blood flow

1) Myogenic theory
2) Metabolic theory
3) Autoregulation

156

Myogenic theory of BP control

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

157

Metabolic theory of BP control

Metabolic activity causes release of vasodilator substances

158

Mechanisms under metabolic theory of BP control

1) O2/nutrient lack theory
2) Vasodilator theory

159

O2 lack theory of BP control

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

160

Nutrient lack theory of BP control

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

161

Vasodilator theory of BP control

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

162

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

Reactive hyperemia

163

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

Active hyperemia

164

Autoregulatory mechanism: Kidneys

Tubuloglomerular feedback

165

Autoregulatory mechanism: Brain

Response to CO2 and H levels

166

Autoregulatory mechanism: Heart

Response to perfusion pressure

167

Mechanism for long-term control of LOCAL blood flow

Angiogenesis

168

Susbtances that cause angiogenesis (3)

1) VEGF
2) FGF
3) Angiogenin

169

Angiogenesis occurs in response to

Hypoxia

170

Vascularity is determined by

MAXIMUM blood flow need

171

Most potent vasoconstrictor

ET-1

172

Vasodilator substance that counteracts TXA2

PGI2

173

Vasodilator vs vasoconstrictor: NE

Vasoconstrictor

174

Vasodilator vs vasoconstrictor: Epi

Vasoconstrictor

175

Vasodilator vs vasoconstrictor: ANP

Vasodilator

176

Vasodilator vs vasoconstrictor: H

Vasodilator

177

Vasodilator vs vasoconstrictor: CO2

Vasodilator EXCEPT at pulmonary vascular bed

178

Vasodilator vs vasoconstrictor: PGF

Vasoconstrictor

179

Vasodilator vs vasoconstrictor: K

Vasodilator

180

Vasodilator vs vasoconstrictor: TXA2

Vasoconstrictor

181

Vasodilator vs vasoconstrictor: ATII

Vasoconstrictor

182

Vasodilator vs vasoconstrictor: PGE

Vasodilator

183

Vasodilator vs vasoconstrictor: Lactate

Vasodilator

184

Vasodilator vs vasoconstrictor: Adenosine

Vasodilator

185

Vasodilator vs vasoconstrictor: Bradykinin

Arteriolar vasodilator, venous vasoconstrictor

186

Vasodilator vs vasoconstrictor: Histamine

Arteriolar vasodilator, venous vasoconstrictor

187

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

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

188

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

Skin