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Cardiac > Cardiovascular Anatomy and Physiology > Flashcards

Cardiovascular Anatomy and Physiology Flashcards

1
Q

Ability to generate an action potential spontaneously

A

Automaticity

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2
Q

Ability to respond to an electrical stimulus by depolarizing and firing an action potential

A

Excitability

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3
Q

Difference in electrical potential between the inside and outside of the cell

A

Resting membrane potential (RMP)

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4
Q

Movement of a cell’s membrane potential to a more postitive value

A

Depolarization

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5
Q

Voltage change that must occur to initiate depolarization

A

Threshold potential

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6
Q

The return of a cell’s membrane potential towards a more negative value after depolarization

A

Repolarization

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7
Q

The movement of a cell’s membrane potential to a more negative value beyond the baseline RMP

A

Hyperpolarization

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8
Q

What features are unique to cardiac myocytes?

A

Intercalated discs form gap junctions that facilitate the spread of action potentials

They contain more mitochondria than skeletal muscle cells (consume O2 at ~8-10mL O2/100g/min at rest)

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9
Q

The ability to transmit electrical current

A

Conductance

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10
Q

Inotropy

A

The force of myocardial contraction during systole

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11
Q

Chronotropy

A

Heart rate

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12
Q

Dromotropy

A

Conduction velocity through the heart (V= D/T)

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13
Q

Lusitropy

A

The rate of myocardial relaxation during diastole

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14
Q

What three factors determine RMP?

A

Chemical force (concentration gradient)

Electrostatic counterforce

Sodium/ potassium ATPase

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15
Q

The primary determinant of RMP

A

Serum potassium

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16
Q

How does decreased serum potassium affect the RMP

A

It decreases the RMP (becomes more negative)

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17
Q

How does increased serum potassium affect the RMP

A

It increases the RMP (becomes more positive)

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18
Q

What is the primary determinant of threshold potential?

A

Serum calcium

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19
Q

How does decreased serum calcium affect threshold potential?

A

It decreases the threshold potential (becomes more negative)

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20
Q

How does increased serum calcium affect threshold potential?

A

It increases the threshold potential (becomes more positive)

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21
Q

How do cells depolarize?

A

Sodium or calcium enter the cell

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22
Q

What is the all or none phenomenon of depolarization?

A

Once depolarization starts, it cannot be stopped

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23
Q

What determines the cell’s ability to depolarize?

A

The difference between RMP and TP

When the two are closer, the cell is more easily depolarizes

When the two are further away, it is more difficult for the cell to depolarize

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24
Q

How does repolarization take place? (electrolytes)

A

Either potassium leaves the cell or chloride enters the cell

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25
Q

The cell’s resistance to subsequent depolarization

A

Refractory period

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26
Q

What functions does the Na/K-ATPase pump serve?

A

In excitable tissue, it restores the ionic balance towards RMP

Removes the Na+ that enters the cell during depolarization

Returns K+ that has left the cell during repolaraization

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27
Q

What is the ratio of Na+ to K+ that the Na/K ATPase pump moves?

A

3 Na+ ions out
2 K+ ions in

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28
Q

What positive inotrope inhibits the Na/K ATPase pump?

A

Digoxin

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29
Q

How does severe hyperkalemia affect Na+ channels?

A

Na+ channels are inactivated

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30
Q

Why is calcium given to hyperkalemic patients?

A

Reduces the risk of dysrhythmias by increasing the gap between RMP and threshold potential

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31
Q

What two parts of the cardiac electrical system do not have a plateau phase?

A

SA node
AV node

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32
Q

What is the normal RMP of the myocyte?

A

-90mV

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33
Q

What is the normal threshold potential of the myocyte?

A

-70mV

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34
Q

Phase of myocyte action potential characterized by activation of fast Na+ channels

A

Phase 0, depolarization

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35
Q

Phase of myocyte action potential characterized by inactivation of Na+ channels; Cl- and K+ channels open

A

Phase 1, initial repolarization

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36
Q

Phase of myocyte action potential characterized by activation of slow Ca++ channels–> delays repolarization –> fast Na+ channels remain inactivated–> refractory period prolonged

A

Phase 2, Plateau phase

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37
Q

Phase of myocyte action potential characterized by K+ leaving the cell faster than Ca++ enters; slow Ca++ channels deactivate–> RMP restored

A

Phase 3, final repolarization

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38
Q

Phase of myocyte action potential characterized by K+ leak channels opening and Na+/K+ ATPase pump maintaining RMP

A

Phase 4, resting phase

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39
Q

What are the phases of the SA node action potential?

A

Phases 4, 0, and 3 (there is no phase 1 or 2)

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40
Q

What phase of the SA node action potential includes:

leaky Na+ channels leading to progressive positivity (funny channels)

T-type Ca++ channels open –> further depolarization

A

Phase 4

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41
Q

What phase of the SA node is characterized by:

Ca++ entry via L-type channels
Depolarization
Na+ channels close
Ca++ T-type close

A

Phase 0

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42
Q

How are T-type and L-type Ca++ channels different?

A

L-type: voltage gated channels, long lasting

T-type: transient, not long lasting

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43
Q

What phase of the SA node action potential is characterized by:

K+ channels opening > K+ efflux > repolarization > decreased Ca++ conductance by closing L-type Ca++ channels

A

Phase 3

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44
Q

What determines heart rate?

A

Intrinsic firing rate

Autonomic tone

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45
Q

What is the intrinsic firing rate of the SA node?

A

70-80 bpm (faster in the denervated heart)

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46
Q

What is the intrinsic firing rate of the AV node?

A

40-60 bpm

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47
Q

What is the intrinsic firing rate of the Purkinje fibers?

A

15-40 bpm

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48
Q

How do volatile anesthetics affect the SA node?

A

SA node depression = may lead to junctional rhythm

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49
Q

What role does the autonomic nervous system play on the heart rate at rest?

A

Parasympathetic tone dominates

Vagus nerve (CN 10)

R vagus nerve innervates the SA node, and the L vagus innervates the AV node

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50
Q

Where does the sympathetic nervous system exert its effect on the heart rate?

A

Via the cardiac accelerator fibers (T1-T4)

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51
Q

What are the SNS effects on heart rate?

A

Norepinephrine stimulates beta-1 receptor > increases Na+ and Ca++ conductance > increases heart rate

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52
Q

How does the SNS effect on HR affect the SA node action potential slope?

A

Phase 4 depolarization slope is steeper

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53
Q

What are the PNS effects on heart rate?

A

Acetylcholine stimulates the muscarinic-2 receptor > increases K+ conductance > hyperpolarization in the SA node > HR decreases

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54
Q

How does the PNS effect on HR affect the SA node action potential slope?

A

Resting membrane potential and reduce the slope of phase 4 depolarization- slope is less steep

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55
Q

What is the equation for oxygen delivery (DO2)?

A

DO2 = cardiac output x [(hgb x SaO2 x 1.34) + (PaO2 x 0.003)] x 10

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56
Q

The amount of gas dissolved in a solution follows what law?

A

Henry’s Law

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57
Q

What is the formula for oxygen content (CaO2)?

A

CaO2 = (Hgb x SaO2 x 1.34) + (PaO2 x 0.003)

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58
Q

What is normal cardiac output?

A

5-6 L/min

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59
Q

What is normal stroke volume?

A

50-100 mL/ beat

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60
Q

What is normal ejection fraction?

A

60-70%

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61
Q

What is normal mean arterial blood pressure?

A

70-105 mmHg

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62
Q

What is normal systemic vascular resistance?

A

800-1,500 dynes sec cm-5

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63
Q

What is normal pulmonary vascular resistance?

A

150-250 dynes sec cm-5

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64
Q

Formula for cardiac output

A

HR x SV

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65
Q

Formula for cardiac index

A

CO/ BSA

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66
Q

Formulas for stroke volume

A

EDF- ESV

CO x (1,000/ HR)

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67
Q

Formula for stroke volume index

A

SV/ BSA

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68
Q

Normal cardiac index

A

2.8-4.2 L/min per m2

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69
Q

Normal stroke volume index

A

30-65 mL/ beat per m2

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70
Q

Formulas for ejection fraction

A

[(EDV-ESV)/ EDV] x 100

(SV/EDV) x 100

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71
Q

Formulas for mean arterial blood pressure

A

(1/3 x SBP) + (2/3 x DBP)

[(CO x SVR)/ 80)] + CVP

72
Q

Formulas for pulse pressure

A

SBP- DBP

Stroke volume output/ Arterial tree compliance

73
Q

Normal pulse pressure

A

40 mmHg

74
Q

Formula for systemic vascular resistance

A

[(MAP - CVP)/ CO] x 80

75
Q

What is the normal systemic vascular resistance index

A

1,500 - 2,400 dynes sec cm-5 per m-5

76
Q

Formula for systemic vascular resistance index

A

[(MAP - CVP)/ CI] x 80

77
Q

Formula for pulmonary vascular resistance

A

[(MPAP - PAOP)/ CO] x 80

78
Q

What is normal pulmonary vascular resistance index?

A

250 - 400 dynes se cm-5 per m2

79
Q

Formula for pulmonary vascular resistance index

A

[(MPAP - PAOP)/ CI] x 80

80
Q

What is the functional unit of the contractile tissue in the heart?

A

Sarcomere

81
Q

What is preload?

A

Ventricular wall tension at the end of diastole just prior to contraction

Volume that returns to the heart during diastole

82
Q

What factors influence preload?

A

Blood volume
Atrial kick
Venous tone
Intrapericardial pressure
Intrathoracic pressure
Body position
Valvular regurgitation (increases)

83
Q

The relationship between volume and pressure can be changed by what?

A

Anything that alters compliance (ie ischemia, hypertrophy)

84
Q

What is contractility (inotropy)?

A

The ability of the myocardial sarcomeres to perform work (shorten and produce force)

85
Q

What percentage of left ventricular end diastolic volume is from atrial kick?

A

20-30%

86
Q

What conditions are associated with reduced myocardial compliance?

A

Myocardial hypertrophy

Heart failure with preserved EF (diastolic failure)

Fibrosis

Aging

87
Q

How does reduce compliance affect ventricular filling?

A

It is more dependent on atrial kick to fill the ventricle and generate a sufficient stroke volume

88
Q

How do preload and after load affect contractility (inotropy)?

A

Contractility is independent of preload and afteroad

89
Q

What factors increase contractility?

A

SNS stimulaiton
Catecholamines
Calcium
Digitalis
Phosphodiesterase inhibitors

90
Q

What factors decrease contractility?

A

Myocardial ischemia
Severe hypoxia
Acidosis
Hypercapnia
Hyperkalemia
Hypocalcemia
Volatile anesthetics
Propofol
Beta-blockers
Calcium channel blockers

91
Q

How does beta-1 stimulation increase contractility?

A

Activates adenylate cyclase > ATP converts to cAMP > cAMP increases activation of protein kinase A (PKA) > activated PKA phosphorylates proteins = :

-L-type Ca++ channels activated (more calcium in the cell)

-Stimulates RyR2 to release more Ca++

-Stimulates SERCA2 to increase Ca++ uptake > enhanced Ca++ release

92
Q

What is the primary substance that determines inotropy?

A

Calcium

93
Q

What is afterload?

A

The force that the ventricle must overcome to eject its stroke volume

94
Q

What factors decrease stroke volume?

A

Decreased preload
Decreased contractility
Increased afterload

95
Q

What hemodynamic measurement is used as a surrogate for afterload?

A

Systemic vascular resistance

96
Q

What does SVR measure?

A

Arteriolar tone

97
Q

Why does SVR not directly measure afterload?

A

It does not account for blood viscosity, blood density, or ventricular wall tension

98
Q

What conditions can set the afterload proximal to the systemic circulation?

A

Aortic stenosis
Coarctation of the aorta

99
Q

What law explains how afterload affect myocardial wall stress?

A

Law of LaPlace

100
Q

According to the Law of LaPlace what factors reduce wall stress?

A

Decreased intraventricular pressure

Decreased radius

Increased wall thickness

101
Q

What is wall stress?

A

The force that holds the heart together

102
Q

What is intraventricular pressure?

A

The force that pushes the heart apart

103
Q

What is the relationship between wall stress and myocardial oxygen consumption?

A

Directly proportional: anything that increases wall stress increases myocardial oxygen consumption

104
Q

Identify coronary artery A

A

Right coronary artery

105
Q

Identify coronary artery B

A

Posterior descending artery

106
Q

Identify coronary artery C

A

Left anterior descending artery

107
Q

Identify coronary artery D

A

Circumflex artery

108
Q

Identify coronary artery E

A

Left coronary artery

109
Q

What are the two divisions of the left coronary artery?

A

Left anterior descending artery

Circumflex

110
Q

Which portions of the heart does the left anterior descending artery perfuse?

A

Anterolateral and apical walls of the LV

Anterior two-thirds of the interventricular septum

111
Q

Which portions of the heart does the circumflex artery perfuse?

A

Left atrium

Lateral and posterior wall of the LV

112
Q

Which portions of the heart does the right coronary artery perfuse?

A

Right atrium

Right ventricle

Interatrial septum

Posterior third of the interventricular septum

113
Q

Which portions of the heart does posterior descending artery perfuse?

A

Inferior wall

114
Q

What determines coronary dominance?

A

The origin of the posterior descending artery

115
Q

What is right coronary artery dominance?

A

The posterior descending artery originates from the right coronary artery

Present in 70-80% of patients

116
Q

What is left coronary dominance?

A

The posterior descending artery originates from the circumflex

117
Q

What is co-dominance?

A

The posterior descending artery originates from the circumflex and right coronary artery

118
Q

What coronary artery supplies the sinoatrial node in MOST patients?

A

Right coronary artery

119
Q

What coronary artery supplies the atrioventricular node in MOST patients?

A

Right coronary artery

120
Q

What coronary artery supplies the Bundle of His in MOST patients?

A

Left coronary artery

121
Q

What coronary artery supplies the left and right bundles branches?

A

Left coronary artery

122
Q

What coronary vein does A represent?

A

Anterior cardiac vein

123
Q

What coronary vein does B represent?

A

Middle cardiac vein

124
Q

What coronary vein does C represent?

A

Great cardiac vein

125
Q

What structure does D represent?

A

Coronary sinus

126
Q

Where does most of the blood returning from the left ventricle drain?

A

Coronary sinus

127
Q

Where does most of the blood returning from the right ventricle drain?

A

Empty directly into the right atrium via the anterior cardiac veins

128
Q

What are the Thebesian veins?

A

They empty a small amount of deoxygenated blood into all four chambers of the heart

129
Q

Explain the anatomic shunt caused by the Thebesian veins.

A

Blood that returns to the left side of the heart via the Thebesian veins dilutes the PaO2 of the blood that is returning from pulmonary circulation.

130
Q

On a 12 lead EKG, which leads correlate with the RCA?

A

Inferior:
II, III, aVF

131
Q

On a 12 lead EKG, which leads correlate with the circumflex?

A

Lateral:
I, aVL, V5, V6

132
Q

On a 12 lead EKG, which leads correlate with the LAD?

A

Septal:
V1, V2

Anterior:
V3, V4

133
Q

What is the best TEE view for diagnosing left ventricular ischemia?

A

Midpapillary muscle level in short axis

134
Q

What law defines coronary blood flow?

A

Ohm’s law

135
Q

Coronary blood flow value

A

225-250 mL/min

136
Q

What is the equation for coronary blood flow?

A

CBF = coronary perfusion pressure / coronary vascular resistance

137
Q

What is the equation for coronary perfusion pressure?

A

Coronary perfusion pressure = Aortic DBP - LVEDP

138
Q

What is coronary reserve?

A

The difference between coronary blood flow at rest and maximal dilation.

139
Q

What is autoregulation of coronary blood flow?

A

Constant coronary blood flow over a range of perfusion pressures between a MAP of ~60 - 140 mmHg.

140
Q

How does coronary blood flow change outside of autoregulation range?

A

It becomes dependent on coronary perfusion pressure

141
Q

How is coronary autoregulation different in atherosclerotic vessels?

A

Maximum dilation may be present at rest = in the setting of increased O2 demand the vessels cannot dilate further > decreased coronary reserve

142
Q

What three factors contribute to autoregulation of coronary blood flow?

A

Local metabolism
Myogenic response
Autonomic nervous system

143
Q

What is the most important determinant of coronary vessel diameter?

A

Local metabolism

144
Q

As myocardial volume oxygen consumption increases, the endothelium releases what vasodilators?

A

Nitric oxide
Prostaglandins
Hydrogen
Potassium
Carbon dioxide

145
Q

What benefits does vasodilation have for the heart during increased myocardial volume oxygen consumption?

A

Decreases vascular resistance
Increases coronary perfusion
Flushes out products of metabolism

146
Q

When does the autonomic nervous system prevail over local metabolism in control of coronary vessel diameter?

A

Vasospastic myocardial ischemia (variant angina)- overactive coronary alpha receptors >intense vasoconstriction> chest pain (always at rest)

147
Q

Coronary artery vasodilation or Constriction:
Histamine- 1

A

Vasoconstriction

148
Q

Coronary artery vasodilation or constriction:
Muscarinic stimulation

A

Vasodilation (d/t nitric oxide)

149
Q

Coronary artery vasodilation or constriction:
Beta-2 (endocardial)

A

Vasodilation

150
Q

Coronary artery vasodilation or constriction:
Alpha (epicardial)

A

Vasoconstriction

151
Q

Coronary artery vasodilation or constriction:
Histamine-2

A

Vasodilation

152
Q

Which waveform correlates with right coronary artery flow?

A

C

153
Q

Which waveform correlates with aortic pressure?

A

A

154
Q

Which waveform correlates with left coronary artery flow?

A

B

155
Q

Why does right coronary artery flow remain constant relative to left coronary artery flow?

A

The right ventricle does not generate enough pressure to occlude blood flow during systole

156
Q

Which myocardial arterial bed is most susceptible to ischemia?

A

Endocardial blood vessels

157
Q

When do most perioperative myocardial infarctions occur?

A

Between 24-48 hours following surgery

158
Q

What conditions both increase oxygen demand and decrease oxygen supply?

A

Tachycardia
Increased preload

159
Q

At rest, what percentage of delivered oxygen does the myocardium consume?

A

70%

160
Q

What is normal coronary sinus oxygen saturation?

A

30%

161
Q

Regulation of vascular smooth muscle tone is dependent on what factors?

A

Autonomic nervous system
Renin- angiotensin- aldosterone system
Local metabolism
Myogenic response

162
Q

What cellular pathways affect intracellular calcium concentration?

A

G-protein cAMP pathway
Nitric oxide cGMP pathway
Phospholipase C pathway

163
Q

What cellular pathway(s) result(s) in vasodilation?

A

G-protein cAMP pathway
Nitric oxide cGMP pathway

164
Q

What cellular pathway(s) result(s) in vasoconstriction?

A

Phospholipase C pathway

165
Q

In the vascular muscle cell, how does increased protein kinase A affect intracellular calcium concentration?

A

Decreases

166
Q

In the cardiac myocyte, how does increased protein kinase A affect intracellular calcium concentration?

A

Increases

167
Q

In what ways does protein kinase-A affect excitation-contraction coupling in the vascular smooth muscle?

A

Inhibition of voltage-gated Ca++ channel in the sarcolemma

Inhibition of Ca++ release from the sarcoplasmic reticulum

Reduced sensitivity of the myofilaments to Ca++

Facilitation of Ca++ reuptake into the sarcoplasmic reticulum via the SERCA 2 pump

168
Q

What factors/ substances increase the production of nitric oxide?

A

Acetylcholine
Substance P
Bradykinin
Serotonin
Vasoactive intestinal peptide
Shear stress

169
Q

What enzyme catalyzes the conversion of L-arginine to nitric oxide in the first step of the nitric oxide cGMP pathway?

A

Nitric oxide synthetase (NOS)

170
Q

What activates the phospholipase C pathway?

A

Phenylephrine
Angiotensin 2
Endothelin-1

171
Q

The phospholipase C pathway increases the production of what second messengers?

A

Inositol triphosphate (IP3)
Diacylglycerol (DAG)

172
Q

Normal DO2 value

A

1,000 mL O2/min

173
Q

Solution coefficient for dissolved oxygen

A

0.003

174
Q

Normal CaO2 value

A

20 mL/dL

175
Q

Venous oxygen content equation

A

CvO2 = (Hgb x SvO2 x 1.34) + (PvO2 x 0.003)

176
Q

Normal CvO2

A

15 mL/dL

Cardiac (4 decks)

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