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E1 Flashcards

1
Q

What is PGC-1 alpha?

A

Key regulator of the body’s response to exercise

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2
Q

What are the systemic effects of PGC-1 alpha?

A

Skeletal muscle hypertrophy, hyperplasia, fiber type switching

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3
Q

What are the cardiac effects of PGC-1 alpha?

A

Metabolism for oxidative phosphorylation and mitochondrial biogenesis

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4
Q

How do you measure maximal oxygen consumption during exercise?

A

Measure VO2 max

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5
Q

What percentage of cardiac output is delivered to skeletal muscle during exercise?

A

85-90%

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6
Q

At peak exercise, what is the ventilation rate?

A

15-25x the starting rate

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7
Q

How does the body reach steady-state conditions during exercise?

A

Progressive increase in heart rate with decrease in stroke volume and mean arterial pressure

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8
Q

How does skeletal muscle adapt to heavy resistance training?

A

Training activates Type IIX fibers and many will change from IIX to IIA

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9
Q

How does hypertrophy affect whole muscle growth?

A

Increased protein synthesis and reduced breakdown

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10
Q

How do you calculate VO2 max?

A

Q x (a - VO2 difference)

Flow x Arteriovenous O2 difference

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11
Q

What is a normal expiration volume compared to VO2 during exercise?

A

40-50%

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12
Q

What are the weekly recommendations for physical activity for someone with minimal/moderate physical activity level?

A

30 min x 5 days of moderate intensity

or

25 min x 3 days of vigorous intensity

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13
Q

What are the weekly recommendations for physical activity for someone with optimal/high physical activity level?

A

60 min x 5 days of moderate intensity

or

30 min x 5 days of vigorous intensity

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14
Q

What are the three major components of the Exercise is Medicine initiative?

A

Assess physical activity
Provide counseling
Provide tools for self-management of exercise

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15
Q

Identify factors that are likely to increase the likelihood of a positive physical activity behavior change

A

5 As:

  1. Ask about physical activity status
  2. Advise about specific recommendations related to the patient to become more active
  3. Agree upon specific physical activity goals
  4. Assist with making an action plan or refer to resources
  5. Arrange for a follow-up contact within a few weeks
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16
Q

What is flux?

A

Hydraulic conductivity x [outward driving forces - inward driving forces

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17
Q

What is the equation for flux?

A

Flux = Resistance x [(Hydrostatic force + Interstitial oncotic pressure) - (Rebasorption force + interstitial hydrostatic pressure)]

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18
Q

What is normal capillary hydrostatic force (Pc)?

A

17.3 mmHg

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19
Q

What is normal interstitial oncotic pressure?

A

8 mmHg

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20
Q

What is normal capillary oncotic pressure?

A

28 mmHg

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21
Q

What is intersitital hydrostatic pressure?

A

-3 mmHg

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22
Q

Reabsorptive force is directly related to….

A

Protein concentration in the blood

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23
Q

Why can liver disease result in edema?

A

Reduced production of plasma proteins in the liver

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24
Q

Why can obstruction of venous circulation result in edema?

A

Because of increased capillary pressure resulting from the resistance to flow

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25
Q

What is the cause of edema associated with infection?

A

Blockage of lymphatic drainage preventing removal of extra interstitial fluid

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26
Q

How can allergic reactions or capillary trauma cause edema?

A

By increasing capillary permeability (Kf) and thus allowing plasma proteins to leak into the interstitial space (increasing interstitial oncotic pressure)

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27
Q

How are capillary beds arranged and why?

A

They are arranged in parallel, rather than series, so that changing flow to one organ does not affect other organs.

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28
Q

What two factors determine blood pressure?

A

Volume and vessel

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29
Q

What’s more compliant–arteries or veins?

A

Veins are 20x more compliant because they store most of the body’s blood

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30
Q

What kind of buffers are arteries and veins?

A

Arteries: pressure
Veins: volume

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31
Q

How does vascular compliance change with age?

A

Compliance lost w/ age –> Stiffening arteries –> Lost diastolic pressure

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32
Q

What must be maintained to ensure capillary perfusion?

A

MAP

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33
Q

What determines preload and afterload?

A

Pre: EDV
After: Aortic Pressure or Pulmonary Artery Pressure

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34
Q

What is an index of systolic function?

A

Ejection fraction

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35
Q

What three factors modulate stroke volume?

A

SV CAP: Contractility (+), preload (+), afterload (-)

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36
Q

What is Starling’s Law?

A

The greater the preload, the greater the afterload

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37
Q

What is S1?

A

Mitral and tricuspid

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38
Q

What is S3?

A

Common extra heart sound
Indicates increased ventricular filling
Usually due to CHF

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39
Q

What is mitral regurgitation?

A

When blood flows back into the left atrium from the LV

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40
Q

What is aortic stenosis?

A

When blood flows through tight aortic valve into ascending aorta

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41
Q

Where is aortic stenosis best heard on auscultation?

A

R 2nd interspace, radiates into both carotids

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42
Q

What is the law of LaPlace?

A

Distended ventricles decreases developed pressure

Wall stress = Pr / 2*wall thickness

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43
Q

What is the equation for cardiac work?

A

W = Aortic pressure x SV

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44
Q

Which drugs lower preload? Afterload?

A

PrEload : vEnodilators

Afterload : vAsodilators

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45
Q

How do venodilators work?

A

By changing vessel radius: dilated veins cause blood to pool in the periphery –> decreased venous return to heart –> ventricular radius gets smaller –> heart becomes more efficient

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46
Q

Why do we give diuretics for CHF?

A

Diuretics decrease total blood volume, and therefore venous return.

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47
Q

What is the relationship between systolic interval and contractility?

A

Inverse

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48
Q

What mainly affects systolic and diastolic intervals?

A

Systolic: contractility
Diastolic: HR

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49
Q

What is mean systemic pressure?

A

6.5 mmHg

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50
Q

How does adenosine affect vasculature?

A

Vasodilator
Increased tissue activity degrades ATP to adenosine
Hypoxia depresses ATP formation, adenosine accumulates

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51
Q

How does potassium affect vasculature?

A

Vasodilator
Small amounts accumulate in extracellular space when released during muscle contraction
These small amounts hyperpolarize VSM

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52
Q

How does CO2 affect vasculature?

A

Diffuses into VSM to cause vasodilation
Combines with H2O to release H+
H+ vasodilates by repolarizing VSM potassium channels

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53
Q

What is hyperemia?

A

Increased blood flow due to vasodilation

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54
Q

How does autoregulation work?

A

It changes resistance to keep flow constant despite changing perfusion pressures

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55
Q

How does nitric oxide affect vasculature?

A

Diffuses rapidly into VSM

Activates soluble guanylate cyclase –> converts GTP to cGMP

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56
Q

How is nitric oxide synthesized?

A

From L-arginine by NOS

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57
Q

What is cGMP?

A

Powerful vasodilatory 2nd messenger

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58
Q

How does increased flow affect nitric oxide production?

A

Increases it. Flow causes shear stress on endothelium, which releases NOS

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59
Q

How does prostacyclin affect vasculature?

A

Powerful vasodilator

Stimulates adenylate cyclase activity –> produces cAMP

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60
Q

Which vasodilator is derived from arachidonic acid?

A

Prostacyclin

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61
Q

Which endothelial factor inhibits platelet aggregation?

A

Prostacyclin

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62
Q

How does calcium affect myocytes?

A

Myocyte contraction is calcium-dependent:

Extracellular calcium enters through L-type Ca2+ channel
Binds to ryanodine receptor on sarcoplasmic reticulum, which releases more calcium

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63
Q

What is SERCA?

A

Pumps Ca2+ back into SR using ATPase

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64
Q

What provides the brakes for the SERCA pump?

A

Phospholamban

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65
Q

How does norepinephrine affect myocytes?

A

Increases contractility by increasing calcium

  1. Stimulates beta-1 receptors, which increase cAMP. cAMP stimulates PKA, which activates Ca2+ channels through phosphorylation
  2. NE also stimulates relaxation – PKA deactivates phospholamban through phosphorylation
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66
Q

What is the resting polarization of cardiac cells?

A

-90 mV

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67
Q

What can EKGs tell us?

A 
Impulse initiation/propagation
HR and position
Heart rhythm and conduction
Chamber size
Infarction
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68
Q

What can EKGs NOT tell us?

A

Contractility
Relaxation
EF, pressure, and flow measurements

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69
Q

What is an EKG lead?

A

Time course of voltage change between two electrodes

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70
Q

P wave

A

Atrial depolarization

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71
Q

Q wave

A

Typically seen in MIs, especially recent MIs

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72
Q

R wave

A

Ventricular depolarization

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73
Q

S wave

A

End of ventricular depolarization

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74
Q

T wave

A

Ventricular repolarization

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75
Q

What do inverted T waves indicate?

A

Recent MI

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76
Q

How long should PR interval be?

A

Less than 0.2 seconds (one big box)

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77
Q

How do you calculate rate from an EKG?

A

300 / boxes in R-R interval

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78
Q

What do regular, prolonged PR intervals indicate?

A

1st degree AV block

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79
Q

What do progressively lengthening PR intervals followed by a drop beat indicate?

A

2nd degree AV block, type I (Wenckebach)

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80
Q

Dropped beats that are not preceded by a change in the length of the PR interval indicate _______

A

2nd degree AV block, type II

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81
Q

What is indicated when atria and ventricles beat independently of each other?

A

3rd degree AV block (Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes)

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82
Q

What is atrial natriuretic peptide?

A

Released from atrial myocytes in response to increased blood volume and atrial pressure. Acts via cGMP. Causes vasodilation and decreased Na+ reabsorption at the renal collecting tubule.

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83
Q

What is B-type natriuretic peptide?

A

Released from ventricular myocytes in response to increased tension. Similar physiologic action to ANP, with longer half-life.

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84
Q

What is indicated by prolonged QRS complex with shortened PR interval?

A

Wolf-Parkinson-White (hallmark = delta waves)

85
Q

How is Wolf-Parkinson-White treated?

A

With ablation

86
Q

How do RVH and LVH present on EKG?

A

RVH: large R in anterior precordials
LVH: large R in lateral precordials

87
Q

What are the lateral leads?

A

I, aVL, V5, V6

88
Q

What are the inferior leads?

A

II, III, aVF

89
Q

What are the anterior/septal leads?

A

V1-4

90
Q

Which electrodes are at the left arm?

A

Positive and negative

91
Q

Which electrodes are at the right arm?

A

Both negative

92
Q

Which electrodes are at the foot?

A

Both positive

93
Q

What is the composition of air?

A

21% O2

79% N

94
Q

What determines flow?

A

Pressure

95
Q

Where in the pulmonary system does flow have the highest velocity?

A

Medium bronchi (lowest cross-sectional area, highest velocity)

96
Q

What clears the majority of deposited particles? What does it consist of?

A

Mucociliary transport system (99%)

Three layers: cilia, sol, gel

97
Q

Cilia beat toward the _____

A

pharynx

98
Q

What secretes the sol layer?

A

Pseudostratified columnar epithelium

99
Q

What secretes the gel layer?

A

Goblet cells, Clara cells, submucosal glands

100
Q

Why do smokers have chronic lower respiratory infections?

A

Because smoke impairs macrophages

101
Q

How do alveolar macrophages work?

A

They contain lysozymes, which engulf particles. They are able to migrate to smaller airways.

102
Q

What has the biggest influence on resistance?

A

Radius (Poiseuille’s law)

103
Q

What is Ohm’s law?

A

V=IR –> Flow = Pressure change / Resistance

104
Q

If r decreases by 1/2, R _____ by _______

A

Increases / 16

105
Q

Where is the highest resistance in the pulmonary system?

A

Medium sized bronchi (also has lowest cross-sectional area and highest flow velocity)

106
Q

T/F: alveolar ducts and sacs are smooth muscle

A

False

107
Q

Albuterol mechanism of action

A

Beta-2 agonist –> vasodilation

108
Q

Which receptors are involved in sympathetic dilation of airway smooth muscle?

A

Beta-2

109
Q

How do increased PCO2 and decreased PO2 affect airway smooth muscle?

A

Airway dilation, decreased resistance

110
Q

What is the slope of the P-V curve?

A

Compliance

111
Q

What is normal pulmonary compliance?

A

200 mL/cm H2O

112
Q

How does COPD affect lung walls?

A

Destroys them by increasing compliance, decreasing elasticity, and increasing resistance

113
Q

COPD is most obvious during inspiration or expiration?

A

Expiration –> prolonged as the patient forces air out through obstructed airways

114
Q

How does fibrosis affect the pulmonary system?

A

Thickens alveolar walls by increasing oxygen, increasing elasticity, and decreasing compliance

115
Q

How does surface tension affect compliance? How does surfactant affect surface tension?

A

Decreases

116
Q

Which cells secrete surfactant?

A

Alveolar type II cells

117
Q

When does surfactant form?

A

During weeks 24-35 of gestation

118
Q

What is hysteresis?

A

Difference in P-V curves (compliance) between inspiration and expiration

119
Q

Hysteresis is due to _____ and reduced by _______

A

Surface tension / surfactant

120
Q

2 x surface tension / alveolar radius = _______

A

Pressure

121
Q

What is intrapleural pressure?

A

Pressure in pleural space –> typically negative –> holds lungs open

122
Q

What is transpulmonary pressure?

A

Difference between alveolar pressure and intrapleural pressure

123
Q

What is the transpulmonary pressure during inspiration?

A

High

124
Q

How does pneumothorax affect ventilation?

A

Air enters intrapleural space, destroys pressure gradient –> lung cannot expand, collapses instead

125
Q

What is tidal volume?

A

500 mL – air moving into lung during quiet inspiration

126
Q

Additional air inhaled after tidal volume

A

Inspiratory reserve volume

127
Q

Air breathed out after normal expiration

A

Expiratory reserve volume

128
Q

Air that cannot be breathed out

A

Residual volume

129
Q

IRV + TV =

A

Inspiratory capacity

130
Q

RV + ERV =

A

Functional residual capacity

131
Q

TV + IRV + ERV =

A

Vital capacity

132
Q

IRV +TV + ERV + RV =

A

Total lung capacity

133
Q

What cannot be measured by spirometry?

A

RV, FRC, TLC

134
Q

What are the muscles of inspiration?

A 
DIAPHRAGM
External intercostals
SCM
Anterior serratus
Scalenes
135
Q

What are the muscles of expiration?

A

ABDOMINALS

Internal intercostals

136
Q

What provides long-term blood pressure regulation?

A

Kidneys

137
Q

What provides acute blood pressure regulation?

A

Nervous system

138
Q

Sympathetic neurotransmitter

A

NE

Epi

139
Q

Parasympathetic neurotransmitter

A

Acetylcholine

140
Q

How does acetylcholine affect vasculature?

A

Endothelium-dependent vasodilator (releases NOS)

141
Q

Sympathetic receptors

A

Andrenergic:
Alpha-1 : vessels
Beta-1 : heart

142
Q

Parasympathetic receptors

A

Cholinergic:

Muscarinic (M-2) : heart

143
Q

Arterial contraction increases ______

A

TPR

144
Q

Venous contraction increases ______

A

VR (and CO)

145
Q

How do beta receptors affect contractility?

A

Increase. Beta receptors increase cAMP, activate PKA, and open Ca2+ channels

146
Q

How do parasympathetics stimulate blood vessels?

A

There is no parasympathetic stimulation of blood vessels

147
Q

What is a potential side effect of beta blockers?

A

Orthostatic hypotension

148
Q

What is the baroreceptor reflex?

A

Increased pressure = increased stretch = increased firing

149
Q

Where are baroreceptors located?

A

High pressure areas: aortic arch, carotid sinus

150
Q

How does hypertension affect baroreceptors?

A

BRs lose sensitivity if BP is constantly high and are therefore less effective at buffering acute BP changes

151
Q

How do baroreceptors affect vasculature?

A

Decreased blood pressure = decreased BR stretch, so BRs DON’T fire. ANS is activated, sympathetics stimulated and parasympathetics inhibited.

SNS: increased HR and contractility
PNS: increased HR (because parasympathetic system is inhibited)

152
Q

Where are cardiopulmonary stretch receptors located?

A

Low pressure areas: atria, pulmonary arteries

153
Q

How do cardiopulmonary stretch receptors work?

A

They sense increased blood volume by measuring filling pressure.

154
Q

What is the Bainbridge reflex?

A

If P increases, HR will increase due to atrial pressure

155
Q

What is the renal response to atrial volume?

A

Reduces fluid levels

  • -Decreased ADH secretion (enhanced fluid excretion)
  • -Dilation of renal arteries
  • -Release of ANP (promotes Na+ excretion and therefore fluid excretion)
156
Q

What is the Cushing reflex?

A

Increased intracranial P increases MAP

Must have MAP>P(IC) for perfusion of the brain

157
Q

The Cushing reflex can trigger _______

A

bradycardia

158
Q

Acute HTN + Bradycardia =

A

Brain injury

159
Q

What is physiologic dead space?

A

The amount of alveolar tissue capable of participating in gas exchange but unable to because of some physical factor (e.g. lack of blood flow to a region of the lung)

160
Q

What is anatomical deadspace?

A

The portion of the airway that conducts air to the alveoli but cannot participate in gas exchange due to its specific anatomy (e.g. trachea, main bronchi).

161
Q

Which circulation supplies the lung parenchyma?

A

Bronchial

162
Q

What are the three hallmarks of pulmonary circulation?

A
  1. Low pressure / Low resistance
  2. High capacity
  3. Vasoconstriction in response to hypoxia
163
Q

What are the functions of pulmonary circulation?

A

Gas exchange in pulmonary capillaries
Vasoconstriction (ACE)
Filter
Blood reservoir

164
Q

Where is ACE present in the pulmonary system and what does it do?

A

Present in endothelial cells in pulmonary capillary beds

Converts angiotensin I to angiotensin II

165
Q

What is PVR?

A

PVR = pulmonary vascular resistance = pressure gradient

166
Q

PVR =

A

(Pulm artery pressure - Left atrial pressure) / CO

167
Q

What is normal pulmonary blood pressure?

A

25/8

artery/capillaries

168
Q

What is pulmonary wedge pressure used for?

A

Estimating LA pressure

Used to assess pulmonary capillary pressure in CHF

169
Q

How do flow and pressure distribute in an upright lung?

A

From top to bottom, P increases, so flow also increases

170
Q

Pressure in lung above and below heart

A

Above: 15 mmHg
Below: 8 mmHg

171
Q

What features of the pulmonary system increase its blood capacity?

A

Thin wall and larger diameter

172
Q

What is the pulmonary system’s circulatory response to hypoxia?

A

Vasoconstriction: low alveolar O2 –> constriction of adjacent vessels

This is to preserve blood for pulm circulation – blood must be ventilated for the body to use

173
Q

What determines the ability of respiratory membrane to transport a gas in/out of blood?

A

Diffusion capacity

174
Q

How does edema affect diffusion rate?

A

Liquid accumulation affects d (distance/thickness)

175
Q

How dos COPD affect diffusion?

A

Decreases diffusion because of decreased surface area of alveoli

176
Q

What is vapor pressure?

A

Partial pressure of H2O in inhaled air

47 mmHg

177
Q

What does vapor pressure depend on?

A

Only on body temperature

178
Q

How is vapor pressure used to calculate partial pressure?

A

PO2 = (760 - 47) x 0.21 = 150 mmHg

179
Q

How is O2 transported in the body?

A

Hemoglobin (97%)

Dissolving (3%)

180
Q

What is P50?

A

PO2 at 50% hemoglobin saturation

181
Q

What causes a right shift in the O2 dissociation curve?

A

ACE BATs right-handed:

Acid
CO2
Exercise
BPG
Altitude
Temperature
182
Q

Bicarb equation

A

CO2 + H2O –> H2CO3 –> H+ + HCO3-

183
Q

Enzyme used to create bicarb

A

Carbonic anhydrase

184
Q

What is the Haldane effect?

A

PO2 increase –> Right shift of CO2 curve

185
Q

What is the Bohr effect?

A

PCO2 increase –> Right shift of O2 curve

186
Q

PCO2 increase causes pH ______

A

Decrease

187
Q

What is normal ventilation perfusion ratio?

A

V(A) / Q = 4.2/5 = 0.8

188
Q

Ventilation perfusion ratio difference between upper and lower lung

A

Upper: > 0.8 (more physiologic dead space)
Lower: < 0.8 (more flow, less air)

189
Q

What is the Alveolar-arterial oxygen gradient?

A

P(AO2) - P(aO2) = 5-15 mmHg

190
Q

What causes the Alveolar-arterial gradient?

A

Bronchial circulation

Imperfect perfusion ratio

191
Q

What is arterial pressure in hypoxemia?

A

< 85 mmHg

192
Q

A-a gradient is normal in _____ and ______

A

High altitude / hypoventilation

193
Q

Arterial PO2 set point

A

100 mmHg

194
Q

PCO2 set point

A

40 mmHg

195
Q

pH set point

A

7.4

196
Q

What controls inspiration and basic ventilation rhythm?

A

Dorsal respiratory group in the medulla

197
Q

What controls expiration?

A

Ventral respiratory group in the medulla

198
Q

What is the pneumotaxic center?

A

Inhibits DRG
Regulates respiratory rate and volume
Located in the medulla

199
Q

Where are central chemoreceptors located?

A

Ventral medulla (not part of respiratory control center)

200
Q

What stimulates central chemoreceptors?

A

Increased H+

Sensitive to PCO2 change in blood. CO2 is able to cross BBB, so it combines with H2O, becomes bicarb, diffuses across BBB, and dissociates into H+

201
Q

What is the most important stimulus of respiratory control centers?

A

Increased arterial PCO2

Major response is in central chemoreceptors, but faster response is in peripheral chemoreceptors

202
Q

What magnifies respiratory response to increased arterial PCO2?

A

Decreased arterial PO2

203
Q

Which respiratory stimulus is important in high altitude / long-term hypoxemia?

A

Decreased arterial PO2

204
Q

What is hypoxemia?

A

Low oxygen in blood

205
Q

Peripheral chemoreceptors are stimulated by ______

A

Decreased arterial pH

206
Q

How does air composition change at high altitude?

A

It doesn’t

207
Q

What are important pressures at sea level?

A

Barometric pressure: 760 mmHg
PH2O (vapor pressure): 47 mmHg
PO2: 150 mmHg
PN2: 563 mmHg

208
Q

How does vapor pressure change with altitude?

A

Does not change in healthy individuals

209
Q

What is the body’s response to high altitudes?

A 
Rapid response: hyperventilation
PCO2 decreases
Respiratory alkalosis
Renal compensation in 1-2 days
Acclimitization

CPR (1 decks)

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