Cardiac physiology, Topnotch Flashcards
1
Q
Blood flow velocty in the aorta
A
11cm/sec
2
Q
Blood flow velocity in the capillaries
A
0.03cm/sec
3
Q
Control conduits for blood flow
A
Arterioles
4
Q
Receptor for venous and arteriolar vasoconstriction in the skin, splanchnic, and renal circulation
A
a1
5
Q
Receptor for arteriolar vasodilation in the skeletal muscles
A
b2
6
Q
T/F: Capillaries undergo vasoconstriction and vasodilation
A
F
7
Q
Law: Blood flow is proportional to pressure difference and inversely proportional to resistance
A
Ohm’s law
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
9
Q
Factors that affect Reynold’s number
A
1) Blood density
2) Blood viscosity
3) Blood flow velocity
4) Blood vessel diameter
10
Q
Laminar vs turbulent: High Reynold’s number
A
Turbulent
11
Q
Highest arterial BP
A
SBP
12
Q
Lowest arterial BP
A
DBP
13
Q
Systolic pressure-diastolic pressure
A
Pulse pressure
14
Q
Central venous pressure is synonymous to ___ atrial pressure
A
Right
15
Q
Pulmonary capillary wedge pressure estimates ___ atrial pressure
A
Left
16
Q
Mean aortic pressure
A
100mmHg
17
Q
Mean arteriolar pressure
A
50mmHg
18
Q
Mean capillary pressure
A
20mmHg
19
Q
Pressure in vena cava
A
4mmHg
20
Q
Glomerular hydrostatic pressure
A
60mmHg
21
Q
ECG: AV node conduction
A
PR segment
22
Q
ECG: Conduction time through AV node
A
PR interval
23
Q
ECG: Ventricular repolarization
A
T wave
24
Q
ECG: Depolarization + repolarization of ventricles
A
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
