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Cardiovascular physiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Size of a current in an ECG is proportional to?

A

Mass of tissue (# of cells)

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2
Q

What medium does an ECG use to detect electrical activity?

A

Extracellular fluid

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3
Q

Which way does the ECG dipole always point?

A

From center of negative electrical field to center of positive electrical field

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4
Q

What does the P wave signify?

A

Atrial depolarization

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5
Q

What does the QRS wave signify?

A

Ventricular depolarization

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6
Q

What does the T wave signify?

A

Ventricular repolarization

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7
Q

What is the PR interval?

A

The beginning of the P wave to the beginning of the QRS wave

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8
Q

How long should a PR interval be?

A

<0.2 sec

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9
Q

What happens if a PR interval is longer than 0.2 sec or shorter than 0.02 sec?

A

Conduction problems from atria to ventricle

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10
Q

How long should the QRS complex be?

A

<0.1 sec

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11
Q

What does it mean if the QRS complex is longer than 0.1sec?

A

-Block in bundle branches
or
-Rhythm originating in ventricular myocytes

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12
Q

What should the ST segment always be?

A

Isoelectric

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13
Q

What happens if the ST segment is not isoelectric?

A

Injury currents which lead to ischemia

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14
Q

What does it mean if the T wave is inverted?

A

Chronic ischemia

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15
Q

Where are the three standard electrode leads?

A

Left and right arms, and left leg

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16
Q

What do the 3 standard electrode leads make up?

A

Einthoven’s triangle

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17
Q

What are the normal axis values for a 12 lead ECG?

A

-30 to 110

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18
Q

What happens with a left axis deviation (<-30)?

A
  • Left ventricular hypertrophy

- Hypertension or cardiomyopathy

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19
Q

What happens with a right axis deviation (>110)?

A
  • Right ventricular hypertrophy

- Pulmonary hypertension disease

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20
Q

What is the sequence of depol in the heart?

A

1) Left septum
2) Septum and endocardium
3) Epicardium
4) Base of heart (Back of left ventricle)

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21
Q

What is the sequence of repol in the heart?

A

1) Epicardium and base repol

2) Endocardium and septum

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22
Q

What is bradycardia?

A

<60 bpm resting heart rate

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23
Q

What is tachycardia?

A

> 100 bpm resting heart rate

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24
Q

Who usually experiences a sinus arrythmia?

A

Young adults and children

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25
Q

What happens to heart rate with sinus arrythmia?

A
  • Faster during inspiration

- Slower during expiration due to parasympathetic activation

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26
Q

What is an arrythmia?

A

Irregular heart rythm

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27
Q

What is a circus rythm?

A

Smaller AP, longer refractory period, and slow conduction velocity due to ischemic area of heart becoming pacemaker

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28
Q

What do injury currents do in myocardial ischemia?

A

Alter the ST segment to elevate or depress it

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29
Q

What cardium is most susceptible to ischemia?

A

endocardium

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30
Q

Why is endocardium more susceptible to ischemia?

A
  • Higher pressures (which squeeze blood vessels)

- Farther from blood supply of coronary arteries

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31
Q

What are the common sites of conduction blocks?

A
  • AV node

- Bundle branches

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32
Q

What are the common causes of conduction blocks?

A
  • Ischemia in the conduction system

- Degenerative changes with age

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33
Q

Is 1st degree heart block life threatening?

A

no

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34
Q

What are the symptoms of 1st degree heart block?

A

none

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35
Q

What happens with 1st degree heart block?

A

Delay of conduction through AV node

->Increased PR interval >0.2 sec

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36
Q

What are the common causes of 1st degree heart block?

A
  • Ischemia
  • Hyperkalemia
  • Drugs that block AV node conduction (Beta blockers, digitalis, Ca blockers)
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37
Q

Is type 1 2nd degree heart block life threatening?

A

No

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38
Q

What happens in type 1 2nd degree heart block?

A

Progressive increase in PR interval until a P wave is not conducted

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39
Q

Is type 2 2nd degree heart block life threatening?

A

Yes

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40
Q

What can treat a type 2 2nd degree heart block?

A

Pacemaker

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41
Q

What happens in a type 2 2nd degree heart block?

A

Series of non-conducted P waves, followed by one conducted P wave

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42
Q

What are symptoms of type 2 2nd degree heart block?

A
  • Very slow HR

- Very slow ventricular depol rate

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43
Q

Where is a 3rd degree heart block found?

A

Between AV node and bundle branches

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44
Q

Is 3rd degree heart block life threatening?

A

Yes

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45
Q

What happens in a 3rd degree heart block?

A

No communication between atria and ventricles which causes

  • Atria: 88 bpm
  • Ventricle: 47 bpm
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46
Q

What are symptoms of 3rd degree heart block?

A

-Fainting (Stokes-Adams attacks)

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47
Q

What can treat 3rd degree heart block?

A

Pacemaker

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48
Q

What type of QRS wave is observed in a Bundle branch block?

A

Wide QRS wave

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49
Q

What does a right bundle branch block do to ventricular depolarization?

A

Causes the last phase of it to extend

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50
Q

What does a Left bundle branch block do to ventricular depolarization?

A

Causes the early phase of it to extend

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51
Q

What can cause a Right bundle branch block?

A
  • Pulmonary hypertension
  • Pulmonary stenosis
  • Elderly degeneration
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52
Q

Is a right bundle branch block life threatening?

A

no

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53
Q

What can cause a Left bundle branch block?

A
  • Systemic hypertension
  • Aortic stenosis
  • Elderly degenration
  • Cardiomyopathy
  • Coronary artery disease
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54
Q

What does a left bundle branch block indicate?

A

Underlying disease

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55
Q

How can a Left bundle branch block be treated?

A

Pacemaker

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56
Q

What happens to the QRS wave and T wave in premature ventricular contraction?

A
  • Wide, irregular QRS

- Inverted T wave

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57
Q

What generates a Premature ventricular contraction?

A

Group of ventricular myocytes

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58
Q

What is a string of Premature ventricular contractions called?

A

Ventricular tachycardia

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59
Q

What are the symptoms of ventricular tachycardia?

A
  • may be no pulse
  • Unconscious in seconds
  • Can be fatal within minutes
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60
Q

What 3 factors effect stroke volume?

A

1) Preload
2) Afterload
3) Contractility

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61
Q

What are the two main mechanisms to increase contractility?

A

1) Frank-Starling mechanism

2) Sympathetic stimulation

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62
Q

Stroke work is directly proportional to?

A

Stroke volume

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63
Q

What happens to the stroke work/ filling pressure chart with sympathetic stimulation?

A

Curve shifts upward and to the left, increases stroke volume with less pressure

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64
Q

What does exercise do to the heart with respect to stimulation?

A
  • Increase SNS stim
  • Venoconstriction
  • Muscle pump
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65
Q

What does exercise do to the heart with respect to stroke volume?

A
  • Increased contractility
  • Increased filling pressure
  • Increased ejection fraction
  • Increased left ventricular end diastolic pressure
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66
Q

Is increase in contractility and/or heart rate enough to increase steady state cardiac output?

A

no

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67
Q

What is required to increase central venous pressure?

A

Coordinated cardiovascular response ( more blood returned to heart)

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68
Q

What is the formula for stroke work?

A

∆P x ∆V

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69
Q

What can exercise do to stroke volume?

A

About double it

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70
Q

What can only SNS stim do to stroke volume?

A

Increase stroke work, but only a little bit of volume

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71
Q

What is the formula for total work of the heart?

A

∆P x ∆V + 1/2mv^2

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72
Q

What is the kinetic work of the heart like at rest?

A

~1% of total work on left side

~5% of total work on right side

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73
Q

What is the kinetic work of the heart like during heavy exercise?

A

~14% of total work on left side

~50% of total work on right side

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74
Q

What is the formula for efficiency of the heart?

A

External work / energy expended

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75
Q

What causes energy expense to be so high in the heart?

A
  • Tension generation

- Ionic pumps

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76
Q

Is efficiency low or high in the heart?

A

Low

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77
Q

What is the formula for energy expense?

A

Time-tension index= Heart Rate x Systolic Blood Pressure

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78
Q

What is the efficiency of the heart at rest?

A

~5-10%

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79
Q

What is the efficiency of the hear during exercise?

A

~15%

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80
Q

About what percent of the hearts energy is used for ionic pumps?

A

~25%

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81
Q

O2 consumption is directly proportional to?

A

Coronary blood flow

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82
Q

What percent of O2 does the heart extract at rest?

A

65-75%

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83
Q

How does coronary blood flow match O2 needs?

A
  • Increased metabolic activity causes cells to release metabolites
  • Coronary vessels vasodilate in response
84
Q

How does coronary blood flow move?

A

-Behind aortic valve-> Sinus of valsalva-> Opening for coronary arteries-> Coronary arteries-> Capillaries-> Veins-> Coronary sinus-> Right atrium

85
Q

What are the three types of flow?

A

1) Laminar
2) turbulent
3) Single file

86
Q

Which layer is the slowest in laminar flow?

A

The outermost layer

87
Q

What is the formula for shear stress?

A

SS=(4 x Flow x Viscosity)/ π x r^3

88
Q

What is shear stress?

A

Frictional force caused by sliding lamina of blood

89
Q

What is an acute adjustment to increased flow and subsequently sheer stress?

A

Dilation to bring ss down to normal level

90
Q

What is a chronic adjustment to increased flow and subsequently sheer stress?

A

remodeling of arteries to become larger

91
Q

What happens if there is very low shear stress?

A

Endothelial cell dysfunction

92
Q

What happens if there is very high sheer stress?

A

Dissecting aneurysm (Tearing of the wall)

93
Q

What are cells subject to low shear stress susceptible to?

A

Atherosclerosis

94
Q

How does the shape of endothelial cells change from high shear stress to low shear stress?

A

More taut with high ss, blocky with low ss

95
Q

What is the formula for the turbulent flow equation (or reynolds #)?

A

Re=(Velocity x diameter x density)/Viscosity

96
Q

At what reynolds number does turbulent flow begin to happen?

A

2000

97
Q

How do the relationship between flow and pressure change once a reynolds number of 2000 is reached?

A
  • Before 2000 is reached Q is directly proportion to P

- After 2000 is reached Q is directly proportional to √P

98
Q

Where is turbulent flow seen?

A
  • Aortic root at peak flow
  • Blood vessel with atherosclerotic plaques
  • Artery branch points
99
Q

Where does single file blood flow happen?

A

Capillaries

100
Q

What is the diameter of a capillary compared to that of a red blood cell?

A

Capillary= 5-6µm

RBC=8µm

101
Q

What is the formula for viscosity of blood?

A

Shear stress/ Shear rate

102
Q

What is the formula for shear rate?

A

∆Velocity/ diameter

103
Q

What is blood serum?

A

Plasma without the clotting factors

104
Q

What is hematocrit?

A

% of red blood cells

105
Q

What is the relationship between hematocrit and viscosity?

A

Hematocrit is directly proportional to viscosity

106
Q

What mainly causes the viscosity of blood?

A

Red blood cells

107
Q

What type of fluid is blood?

A

Non Newtonian fluid

108
Q

How does viscosity relate to the size of the tube in which the liquid is contained?

A
  • The smaller the tube the less viscous the liquid

- The bigger the tube the more viscous the liquid

109
Q

How does viscosity relate to shear rate?

A

As shear rate goes up viscosity goes down

110
Q

How does high shear rate lower viscosity?

A

It keeps RBCs spread out

111
Q

How does low shear rate raise viscosity?

A

It allows RBCs to stick together

112
Q

What happens to hematocrit in microvessels?

A

It decreases from aaroun 40% in central to 24% in arteriolar

113
Q

What is the formula for Pousilles law?

A

Q=(∆P x π x r^4)/ (8 x Viscosity x L)

114
Q

What is the formula for resistance in series?

A

Rtotal= R1+R2+R3…..

115
Q

What is the formula for resistance in series?

A

1/Rtotal=1/R1+1/R2+1/R3….

116
Q

What is the formula for tension?

A

Tension= Pressure x Radius

117
Q

What is the formula for wall stress?

A

Wall stress= (Pressure x radius)/ wall thickness

118
Q

What is the acute vessel reaction to hypertension?

A

Constriction

119
Q

What is the long term vessel reaction to hypertension?

A

Increase in wall thickness

120
Q

What is the formula for Mean Arterial Pressure at rest?

A

MAP= Diastolic BP + (Systolic BP - Diastolic BP)/3

121
Q

What is the usual speed of blood flow?

A

~0.2 m/s

122
Q

What happens to a pressure wave as arteries stiffen?

A

The pressure wave begins to move faster

123
Q

What is the pressure wave difference between someone young and someone old?

A 
Young= ~4-5 m/s
Old= ~10 m/s
124
Q

What effect does a fast pressure wave have on the vascular system?

A

Increases Mean arterial pressure

125
Q

How does venous shape change from low volume to high volume?

A

At very low volume it becomes dumbbell like, works its way up to circular

126
Q

What happens to venous blood when someone goes from supine to standing?

A

Shifts ~500mL blood to the lower extremities

127
Q

What causes hypotension of the veins?

A

Decreased central venous pressure and decreased stroke volume

128
Q

What is the long term compensation to hypotension?

A

Venoconstriction

129
Q

What two factors maintain flow with posture change?

A
  • Increase in arterial pressure

- Increase in Venous pressure

130
Q

What two pumps assist venous flow?

A
  • Respiratory

- Muscle

131
Q

What do muscle and respiratory pumps do to capillary pressure in the foot?

A

Decrease it

132
Q

What happens during a inspiration respiratory pump?

A
  • Decreased pressure in thoracic veins
  • Increased abdominal pressure
  • Increased filling in thoracic veins
133
Q

What happens during a expiration respiratory pump?

A
  • Increased Pressure in thoracic veins
  • Decreased abdominal pressure
  • Decreased filling in thoracic veins
134
Q

What are the 4 regulated Hemodynamic factors?

A

1) MAP
2) Tissue flow
3) Shear Stress
4) Wall Stress

135
Q

What is the formula for MAP?

A

MAP= Q x Total peripheral resistance

136
Q

What regulates Tissue flow?

A

∆ing artery/arteriole diameter

137
Q

What regulates shear stress?

A

Artery/arteriole diameter

138
Q

What regulates wall stress?

A
  • Artery/arteriole diameter acutely

- Wall thickness chronically

139
Q

Where does endothelial cell paracellular transportation happen?

A

Between junctions

140
Q

Where does endothelial cell transcellular transportation happen?

A

Through the actual cell

141
Q

Describe endothelial cells on the arterial side

A
  • Elongated with prominent stress fibers

- Low permeability (complex tight junctions)

142
Q

Describe endothelial cells on the venous side

A
  • Have receptors for inflammation

- Very leaky when inflammation occurs

143
Q

Name the type of capillaries by premeability from lowest to highest.

A

Lowest: Continuous
Mid: Fenestrated
Highest: Discontinuous

144
Q

What are the main inflammatory factors?

A
  • VEGF
  • Histamine
  • Substance P
145
Q

What do the inflammatory factors do?

A

Increase permeability on the venous side

146
Q

What does a rise in cAMP do?

A

Decrease permeability by increasing tight junction formation

147
Q

What does a rise in cGMP do?

A

Increase permeability

148
Q

What does an increase in shear stress do?

A
  • Acutely increases permeability

- Chronically decreases permeability

149
Q

Where are vesicula-vacular organelles found?

A

In venules within tumors or areas of high inflammation

150
Q

How does VVO permeability compare to caveolae permeability?

A

About 2 x as wide as caveolae and much more permeable

151
Q

What inflammation factors are normally found where VVOs are?

A
  • VEGF*
  • Serotonin
  • Histamine
152
Q

How do endothelial cells control blood vessel diameter?

A

Release of vasoactive factors

153
Q

What 3 vasoactive factors relax smooth muscle cells?

A

1) NO* (nitric oxide)
2) PGI2 (prostacyclin)
3) EDHF (Endothelial derived hyperpolarizing factor)

154
Q

How does EDHF move from ECs to SMCs?

A

Through gap junction

155
Q

What vasoactive factor constricts smooth muscle cells?

A

Endothelin

156
Q

What two channels do endothelial cells have?

A
  • ATP K/NA channel (Na-K ATPase)

- Kir (inward rectifier potassium channel)

157
Q

What is the range of a EC resting membrane potential?

A

-30 to -68 mV

158
Q

Why do ECs not have action potentials?

A

No voltage gated Na or Ca channels so no upstroke

159
Q

What is IP3?

A

Inositol triphosphate

-A membrane phospholipid metabolite

160
Q

What two things does an increase in EC Ca do?

A

1) Activates Nitric Oxide synthase-> release NO-> SMC relaxation
2) Increases permeability in venules

161
Q

What does hyperpolarization of a EC do?

A

1) Increases the driving force for Ca entry

2) Travels from EC-> SMC to hyperpolarize it-> relaxation

162
Q

How does PGI2 move from ECs to SMCs?

A

Uses a g protein receptor (7 crossing)

163
Q

What is Prostacyclin (PGI2)?

A

A metabolite of arachidonic acid which is a membrane phospholipid derived molecule

164
Q

What is COX?

A

Cyclo Oxygenase

165
Q

What does aspirin (a NSAID) do?

A

Blocks COX from converting arachidonic acid to PGI2

166
Q

How is PGI2 made?

A

PLA2->arachidonic acid -COX> PGI2

167
Q

What are NO*s 4 anti-atherosclerotic effects?

A

1) Relaxes SMC
2) Inhibits platelet aggregation
3) Inhibits EC and SMC proliferation
4) Inhibits luekocyte adhesion

168
Q

What is NO*s non anti-atherosclerotic effect?

A

-Involved in increased venular permeability with inflammation

169
Q

What two things produce NO*?

A
  • Shear Stress

- Agonists

170
Q

What is PI3K?

A

PI3 Kinase

171
Q

What is eNOS?

A

Endothelial Nitric oxide synthase

172
Q

How does increased intracellular Ca stimulate eNOS?

A

Increased Ca->Ca-Calmodulin->Binds to eNOS and activates

173
Q

What is the other way (not Ca but still requires calmodulin) to stimulate eNOS?

A

Phosphorylation of eNOS

174
Q

What is EDHF?

A

Probably a metabolite of arachidonic acid

175
Q

What causes dilation in large arteries?

A

Mainly NO, very little EDHF

176
Q

What causes dilation in small arteries and arterioles?

A

Primarily EDHF

177
Q

What is required for EDHF to move?

A

Myoendothelial gap junctions (MEJs)

178
Q

When do Myoendothelial gap junctions increase?

A

With a decrease in arteriole/artery size

179
Q

How long does endothelin constriction last?

A

2-3 hours after washed away

180
Q

What does Endothelin participate in?

A

Remodeling-> Stimulates vascular and cardiomyocyte proliferation-> Participates in hypertrophy

181
Q

What is endothelin implicated in?

A
  • Carcinogenesis
  • Bronchoconstriction
  • Fibrosis
  • Heart failure
  • ***Pulmonary hypertension (Vasoconstriction in lungs)
182
Q

What is ECE?

A

Endothelium converting enzyme

183
Q

What percentages of endothelin go where?

A

25% to Circulation

75% to SMC

184
Q

What can decrease the production of ET-1 mRNA?

A

Increase in NO and PGF2

185
Q

What regulates production of ET-1?

A

Increase or decres in Pre-Pro ET-1

186
Q

What can raise Pre-Pro ET-1?

A
  • Vasoconstrictors (Shear stress, Angiotensin, vasopresin, and catecholamines)
  • LDL
187
Q

What can lower Pre-Pro ET-1?

A

-Vasodilators (NO*, PGI2, atrial natriuretic peptide, estrogen)

188
Q

What does ET-1 usually play a role in?

A

total amount of vasoconstriction in body

189
Q

Where is ET-1 the highest?

A

In the lungs by about 5x

190
Q

What can improve pulmonary hypertension caused by ET-1?

A

Endothelin receptor blockers

191
Q

What is the rate limiting reagent in the RAAS system?

A

Renin

192
Q

How is angiotensin made?

A

Angiotensinogen -renin> Angiotensin I-> Angiotensin II

193
Q

What is ACE?

A

Angiotensin converting enzyme

194
Q

What releases renin?

A

The kidneys

195
Q

What releases angiotensinogen?

A

Liver

196
Q

What releases ACE?

A

Lungs

197
Q

What do ACE inhibitors do?

A

Treat hypertension

198
Q

What does angiotensin II do?

A
  • Increase SNS activity
  • Potent vasoconstriction
  • Increase H2O kidney reabsorption
  • Increase thirst
  • Increase Mean arterial pressure
199
Q

What are the clotting effects after there is a tear or rupture of small blood vessels?

A

-Vascular constriction-> Platelet plug formation-> 3-6 minutes later blood coagulation

200
Q

What is the process of clotting after vessel damage?

A

Vessel damage-> Activates clotting cascade-> activation of thrombin in blood which allows fibrinogen to create an insoluble fiber network

201
Q

What is a thrombus?

A

-Clot attached to blood vessel wall

202
Q

What is a embolus?

A

-Free floating clot

203
Q

What are the 4 main causes for thromboembolisms?

A

1) Imbalance between clotting and anticlotting factors due to atherosclerosis or age
2) Slow moving blood
3) Large mass of traumatized tissue
4) Septicemic shock

204
Q

How can a large mass of traumatized tissue cause a thromboembolism?

A

Widespread clotting

205
Q

How can septicemic shock cause a thromboembolism?

A

Bacterial infection can intitate clotting cascade

206
Q

What are the steps to allow infiltration of leukocytes in venules?

A

1) Acitvated EC
2) Slow rolling
3) Arrest leukocytes
4) Diapedis

Cardiovascular physiology (3 decks)

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