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CPR > Test 5 - pulmonary > Flashcards

Test 5 - pulmonary Flashcards

1
Q

What are the clinical symptoms of brocnhitis? Is fever a common symptom?

A

productive cough

wheezing

fever is unusual

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2
Q

How is bronchitis diagnosed?

A

Clinical diagnosis - based on symptoms of cough, wheezing. CXR is only indicated if pneumonia is suspected, and if consolidation is not seen pneumonia can be ruled out.

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3
Q

What is pneumonia?

A

Infection of the lung parynchyma (respiratory airways)

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4
Q

Pneumonia is categorized into 4 types. Name these 4 types (one type is further divided into two categories)

A

Community acquired (typical and atypical)

Hospital acquired

Health-care associated

Opportunistic

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5
Q

What are the clinical symptoms of pneumonia?

A

fever

chest pain

dyspnea

productive cough

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6
Q

How is pneumonia diagnosed? Is culture often performed?

A

Diagnosis is made with clinical symptoms and a chest x-ray with focal lung opacities

Culture is not usually performed because patients cannot expectorate sputum and even if they can the culture is contaminated with oropharyngeal bacteria

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7
Q

How is pneumonia treated? discuss community-acquired and hospital-acquired treatments

A
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8
Q

What is Mycobacterium tuberculosis? (stain, shape, and type of microbe)

A

Tuberculosis is an acid fast rod bacterium

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9
Q

How is TB transmitted?

A

air droplets

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10
Q

Describe the potential course of TB (primary infection, etc)

A
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11
Q

What are the general clinical symptoms of TB?

A

productive cough

fever

malaise

weight loss

+/- hemoptysis

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12
Q

If TB becomes systemic, what diseases can the patient develop?

A

Pott’s disease (TB in the vertebrae)

Milliary disease (widespread dissemination)

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13
Q

How is active TB diagnosed (there are a few methods you should name)? Can IGRA or a PPD test diagnose active TB?

A

CXR

Sputum smear with acid fast stain (takes 4-6 weeks to culture)

nucleic acid amplification

IGRA and PPD CANNOT diagnose active TB

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14
Q

Is PPD specific to Mycobacterium tuberculosis?

A

If the patient recieved a BCG vaccination, PPD will yield a positive result

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15
Q

How does primary TB and secondary TB present on CXR?

A

Primary TB has cavitary lesions in the lower/middle lobe(s)

Secondary has cavitary lesions in the upper lobe(s)

Note: hilar LAD may be present in both

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16
Q

What are risk factors for developing active TB?

A

Malnutrition

immunocompromized patients (drugs, HIV)

Diabetes

alcoholism

children under 2 years of age

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17
Q

How is TB treated?

A
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18
Q

What type of infectious agent causes pneumocystis pneumonia and in what patient population is this infection seen in?

A

PCP is a fungal pneumonia (caused by Pneumocystis jirovecii) that is commonly seen in AIDS patients with a CD4 count below 200

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19
Q

What are the clinical symptoms of pneumocystis pneumonia?

A

fever

non-productive cough

dyspnea

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20
Q

How is pneumocystis diagnosed?

A

Chest imaging (ground glass opacities) +/- “crushed ping-pong balls” opacities

Bronchoalveolar lavage crushed ping-pong balls morphology

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21
Q

What is the treatment for pneumocystis pneumonia?

A

Bactrim (sulfamethoxazole and trimethoprim)

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22
Q

What is bronchiolitis?

A

Inflammation of the bronchioles

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23
Q

What age is bronchiolitis typically seen in? What are the clinical symptoms of bronchiolitis?

A

Seen in children under 6 months

coryza (stuffy nose)

Rhinorrhea (runny nose)

cough

wheezing

chest wall retractions

respiratory distress

difficulty feeding due to increased work of breathing

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24
Q

How is bronchiolitis diagnosed?

A

CXR:

air trapping

peribronchial thickening

subsegmental opacities

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25
Q

How is bronchiolitis treated?

A

Supportive therapy only:

fluids, O2, bronchodilators

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26
Q

What is laryngeotracheobronchitis?

A

Croup

upper airway obstruction

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27
Q

What causes croup?

A

RSV and parainfluenza

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28
Q

What are the clinical symptoms of croup? Is fever common?

A

Seal bark cough

Stridor (inspiratory wheeze)

hoarsness

fever is not common

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29
Q

How do you diagnose croup? Do you use a tongue depressor to examine the pharynx?

A

Steeple sign on XR

DO NOT stick anything in through as the airway could collapse!!

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30
Q

How is croup treated?

A

For kids in respiratory distress - aerosolized racemic epinephrine reduced subglottic edema

Systemic steroids

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31
Q

What is epiglottitis? What is the most common cause?

A

inflammation of the epiglottis

H. influenzae

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32
Q

What are the clinical symptoms of epiglottitis?

A

fever

drooling

dysphagia

refusal to eat/drink

sudden onset of stridor

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33
Q

How is epiglottitis diagnosed?

A

Thumb sign on XR

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34
Q

How is epiglottitis treated?

A

intubation

antibiotics

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35
Q

Draw the restricive pattern dendritic

A

Notice that hypersensitivity pneumonitis is under granulomatous diseases and inhaled. Inhalation of particles results in non-caseating granulomas

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36
Q

What are the finding in a restricitve pattern? (PFT results)

A
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37
Q

What changes can be seen on a spirogram in restrictive diseases? Are RV and FRC reduced in neuromuscular diseases?

A

RV is normal/high in neruromuscular disease

FRC is normal in neuromuscular disease

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38
Q

What changes can be seen on a flow-volume loop in restrictive diseases?

A
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39
Q

What are the 3 categories (heavily focused on in sullabus) of diffuse parenchymal lung disease?

A

Idiopathic pulmonary fibrosis

granulomatous disease

inhaled disease

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40
Q

What is Idiopathic pulmonary fibrosis?

A

increased flibroblast growth and collagen synthesis in the alveolar interstitium

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41
Q

What are the clinical symptoms of idiopathic pulmonary fibrosis? Is it an acute process? is the prognosis good or bad?

A

exertional dyspnea (decreaed RBC transit time)

dry cough

inspiratory crackles at lung bases (velco sounding)

digital clubbing

It is a slow, insideous process that shows up late in life (poor prognosis)

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42
Q

How does IPF change FEV1, FVC, FEV1/FVC, DLCO, A-a O2 difference

A

reduced FEV1, FVC, DLCO

normal FEV1/FVC

increased A-a O2 difference

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43
Q

How does IPF present on CXR? CT?

A

CXR

low lung volumes, reticulonodular opacities

CT

honeycombing at lung bases

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44
Q

How is IPF diagnosed?

A

history, PFTs, and imaging

biopsy is not always required

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45
Q

How is IPF treated?

A

There are no real treatments for IPF

anti-fibrotic agent prifenidone may help to slow down progression

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46
Q

What diseases are classified under granulomatous restrictive lung diseases?

A

Sarcoidosis

Hypersensitivity pneumonitis

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47
Q

What is sarcoidosis?

A

inflammation process that results in the formation of non-caseating granulomas in the lungs

In severe cases, the disease is systemic

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48
Q

Who is at high risk for sarcoidosis? What organ systems are involved in systemic disease?

A

black women

heart, CNS, liver, spleen, skin, eyes

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49
Q

What are the clinical symptoms of intrapulmonary sarcoidosis? extrapulmonary?

A

Intrapulmonary:

typically asymptomatic

dyspnea

nonproductive cough

Extrapulmonary:

arrhythmias (heart block)

uveitis

hepatomegaly

Lofgren’s syndrome (erythemia nodosum, fever, hilar LAD)

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50
Q

How is sarcoidosis diagnosed?

A

symptoms, CXR, and biopsy of non-caseating granulomas

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51
Q

How is sarcoidosis treated?

A

Disease spontaneously resolves in most patients

For those with severe pulmonary symptoms, corticosteroids are used

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52
Q

What disease closely resembles sarcoidosis?

A

Berylliosis

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53
Q

What is hypersensitivity pneumonitis

A

parenchymal lung disease characterized by non-caseating granulomas brought on by the inhalation of particles (specific particles)

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54
Q

Is HSP reversible?

A

In most cases, yes

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55
Q

What are the clinical symptoms of hypersensitivity pneumonitis?

A

Presents like pneumonia

fever

dyspnea

cough

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56
Q

When do hypersensitivity pneumonitis symptoms present?

A

4-8 hours after exposure

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57
Q

How does HSP present on radiograph? Acute vs Chronic

A

Acute:

ground glass opacities (similar to PCP) with upper lobe predominance

Chronic:

volume loss

reticular opacities

honeycombing

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58
Q

How is hypersensitivity pneumonitis diagnosed?

A

re-expose patient to particle and see if symptoms recur

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59
Q

How is HSP treated?

A

Avoid the antigen

steroids in acute, severe situations

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60
Q

What diseases are classified under inhaled?

A

Hypersensitivity pneumonitis

Asbestosis

Silicosis

Coal Worker’s pneumoconiosis (black lung)

Berylliosis

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61
Q

What is asbestosis?

A

A fibrotic lung disease brought on by the inhalation of asbestos

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62
Q

Who is at risk for asbestosis?

A

occupational hazard:

shipyard/shipbuilding

brak lining work

insulation and textiles

stone polishing and cutting

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63
Q

What is the pathophysiology of asbestos?

A

Fibers are inhaled —> lower resp. tract —> pneumocytes and alveolar macrophages release inflammatory mediators, ROS, free radicals —> progressive fibrosis

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64
Q

How long does asbestosis present after exposure?

A

many years after exposure

65
Q

How does asbestosis present on CXR?

A

bilateral patchy reticular opacities w/ associated calcified pleural plaques

66
Q

How is asbestosis diagnosed?

A

history of exposure, radiology, biopsy (not necessary)

67
Q

How is asbestosis treated?

A

It isn’t. Just monitor for cancer

68
Q

What is silicosis?

A

Pulmonary disease caused by inhalation of crystalline silica - most abundant mineral on earth found in rocks and sandstone

69
Q

Who is at risk for silicosis?

A

Occupational:

sandblasting

masonry

polishing

mining

tunneling

70
Q

What is the pathologic hallmark of silicosis?

A

silicotic nodule

71
Q

What are the clinical features of silicosis?

A

dyspnea

weight loss

fatigue

72
Q

How does silicosis present on CXR?

A

Acute silicosis: basilar-predominant, alveolar opacities

Simple silicosis: small, upper lobe-predominant nodules

Chronic silicosis: coalesced nodules w/ upper lobe fibrosis, hilar adenopathy and calcification

73
Q

How is silicosis diagnosed?

A

history and radiographic findings

74
Q

What is coal worker’s pneumoconiosis?

A

lung disease caused by the inhalation of carbon dust + silica

75
Q

Who is at risk for the black lung?

A

occupational:

coal mining

graphite mining

milling

76
Q

How does the black lung show up on CXR?

A

Maybe small upper lobe nodules

Chronic: coalescence of nodules

77
Q

How is the black lung diagnosed?

A

clinical features

78
Q

How is the black lung treated?

A

supportive therapy

79
Q

Who is at risk for berylliosis?

A

Occupational

metal alloy manufacturing

nuclear industry (hanford)

80
Q

Clinically, what other disease does berylliosis resemble?

A

sarcoidosis

81
Q

What is kyphoscoliosis? What implications does the condition have for pulmonary function?

A

Lateral deviation + kyphosis (concavity w/ respect to the ventral surface) of the spine. It has the effect of increasing chest wall stiffness, causing restriction.

82
Q

How is kyphoscoliosis diagnosed?

A

physical exam

83
Q

How is kyphoscoliosis treated?

A

surgery or braces for young

supportive for old

84
Q

What are the three possible sites for neuromuscular dysfunction in restricitve lung diseases?

A

nervous system

neuromuscular junction

muscle

85
Q

What are clinical features of neuromuscular diseases?

A

muscle weakness

86
Q

How do neuromuscular diseases change PFTs? (RV and FRC) What should be done on PFT to assess strength?

A

RV is normal or high

FRC is slightly decreased

Max inspriratory and expiratory pressures

87
Q

What is usually the cause diaphragmatic weakness?

A

weakness usually from phrenic nerve disruption (C3-5)

88
Q

What are clinical features of diaphragmatic weakness?

A

Unilateral weakness is usually asymptomatic

Bilateral weakness results in dyspnea, which is worse when lying down (orthopnea)

89
Q

How is diaphragmatic weakness diagnosed?

A

upright and supine spirometry (>20% decrease in FVC when supine)

Electromyography

unilateral weakness:

will show elevated hemidiaphragm in CXR

Sniff test to visualize diaphragm under fluoroscopy

90
Q

How is diaphragmatic weakness treated?

A

Diaphragmatic plication: a surgery that fixes the diaphragm in a flat position

Non-invasive ventilation

91
Q

Is it important for the pulmonary vascular system to maintain a low pressure system?

A

yes

92
Q

How is pulmonary artery pressure related to cardiac output and pulmonary vascular resistance? (equation)

A

PAP = CO x PVR

93
Q

Describe recruitment and distention

A

As blood flow increases, intravascular pressures increase which causes initially closed pulmonary vasculature to open (recruitment). In addition, the caliber of already open vessels increase (distention).

94
Q

What is one of the most important vasodilators?

A

Nitric oxide

95
Q

Define hypoxic vasoconstriction

A

Hypoxic pulmonary vasoconstriction (HPV) is a vital mechanism that alters pulmonary vascular resistance and redistributes blood to better ventilated areas of the lung.

96
Q

How does alveolar pressure determine blood flow through capillaries? Discuss using the Starling resistor theory (PA, Pa, Pv)

A
97
Q

Describe how lung volumes affect the caliber of intra and extra-alveolar vessels. Wat is the significance of FCR?

A

low lung volumes = intra vessels are at their greatest caliber while extra are at their smallest

high lung volumes = intra vessels are at their smallest caliber while extra are at their greatest

FCR is where the resistance of intra and extra-alveolar vessels are equal

98
Q

Describe the role of bronchial circulation.

A

Bronchial circulation supplies the lung with oxygen and nutrients and is under systemic pressures becuase it is coming from the systemic circulation

99
Q

Pulmonary hypertension is defined as a mean pulmonary arterial pressure above ___ mmHg.

A

25 mmHg

100
Q

What can cause pulmonary hypertension?

Hint: Mean PAP = (PBF x PVR) + LAP

A
  • Increasing pulmonary vascular resistance (PVR)
    • Most common
  • Increasing pulmonary blood flow (PBF)
    • Only results in hypertension if the effects of recruitment and distention are exhausted
  • Increasing left atrial pressure (LAP)
101
Q

Name the 5 categories of pulmonary hypertension

A

Group 1: Pulmonary arterial hypertension

Group 2: Left heart disease

Group 3: lung diseases

Group 4: chronic thromboembolism

Group 5: miscellaneous

102
Q

What are some common clinical presentations of pulmonary hypertension?

A

Loud P2

Elevated JVP

Prominent a, c, and v waves

Murmur of tricuspid regurgitation

Hepatomegaly (severe)

Ascites (severe)

Lower extremity edema (severe)

103
Q

How does pulmonary hypertension change an ECG?

A

Tall P waves in lead II (suggestive of right atrial enlargement)

Large R wave in V1 (right ventricular hypertrophy)

Right axis deviation

104
Q

How does pulmonary hypertension present on radiography?

A

enlarged pulmonary arteries

right heart enlargment

105
Q

How is pulmonary hypertension treated?

A

treat underlying cause

vasodilators:

calcium channel blockers, PDE inhibitors, endothelin receptor antagonists

106
Q

What is a venous thromboembolism?

A

Venous thromboembolism is a combination of two diseases: deep vein thrombosis (DVT) and pulmonary embolism (PE).

107
Q

What causes 90% of PEs?

A

DVTs

108
Q

How do VTEs affect gas exchange and pulmonary hemodynamics?

A

Gas exchange:

creates dead spaces

Blockage sends more blood (increased Q) to other areas creating low VA/Q areas

Pulmonary hemodynamics

if the block is too big for recruitment and distention mechanisms, PVR will increase

109
Q

What are the 3 major risk factors for VTE?

A

Stasis

Vascular injury

Hypercoagulability

110
Q

What are the clinical symptoms of DVT and PE?

A

DVT

swelling, pain, erythema, warmth

PE

Acute onset of dyspnea, pleuritic chest pain depending on location, cough, hemoptysis, loud P2, tachypnea

111
Q

How is VTE treated?

A

Anticoagulation with heparin and are put on warfarin or LMWH for 3-6 months depending on their risk factor profile

Thrombolytics are reserved for patients with hemodynamic instability and/or cardiac arrest

112
Q

What are arteriovenous malformations?

A

anatomic shunts

Abnormal movement of blood from the systemic venous system to the systemic arterial system without passing through the gas exchanging areas of the lung

113
Q

How do arteriovenous malformations affect gas exchange and pulmonary hemodynamics?

A

Gas exchange

  • Because blood bypasses the pulmonary capillaries, PaO2 and SaO2 will decrease. The amount that a decreases depends on the size of the shunt.

Pulmonary hemodynamics

  • PVR is somewhat reduced, but the amount depends on the size of the shunt. Therefore, a smaller shunt will barely change PVR and a large shunt will have a greater change in PVR
114
Q

What is orthodexia? What causes orthodeoxia?

A

Shunts located at the base of the lungs lead to orthodeoxia

Changing from the supine to the erect posture leads to a redistribution of blood flow which increases the shunt fraction and increases hypoxia

115
Q

What is a paradoxical emboli? Why are patients with an arteriovenous shunt at high risk for one?

A

A paradoxical embolism is formed in the venous system and can move through a shunt into the arterial circulation

116
Q

What are the causes of arteriovenous malformations?

A

atrial/ventral septal defects

malformation of blood vessels

117
Q

What are the clinical symptoms of AVMs?

A

Dyspnea

Orthodeoxia

Platypnea (dyspnea worse in the upright position)

Hypoxemia

Digital clubbing

118
Q

How are AVMs treated?

A

surgery

embolization of vessels feeding the shunt

119
Q

What is hemoptysis?

A

Coughing up blood

120
Q

What are the potential sources of hemoptysis? Which is most common?

A

Bronchial circulation and pulmonary circulation

Bronchial circulation is the most common because it is under systemic arterial pressure.

121
Q

What are some causes of bronchial arterial hemorrhage?

A

Suppurative airway and parenchymal lung diseases

Bronchiectasis

Tuberculosis

Lung abscess

Bronchitis

Neoplasms in the airway (primary or metastasized)

122
Q

What are some causes of pulmonary circulation hemorrhage?

A
  • Autoimmune disorders
    • Inflammatory conditions causing vasculitis within the pulmonary circulation causing diffuse alveolar hemorrhage
  • Vascular disease
    • Pulmonary embolism
    • Pulmonary arteriovenous malformation
    • Pulmonary artery aneurysms
123
Q

What is the Rasmussen’s disorder?

A

In rare cases, TB causes dilation and rupture of a pulmonary artery. This phenomenon is called Rasmussen’s aneurysm

124
Q

What are the clinical symptoms of hemoptysis?

A

hemoptysis

peribronchial cuffing on CXR

125
Q

What is the treatment for hemoptysis?

A

Massive-hemoptysis (200-600 mL/24 hour) ***clinical emergency***

  • Localize the source and embolize the vessel
  • Surgical resection if embolization is not successful

Non-massive hemoptysis

  • Diagnostic workup
    • Bronchoscopy
    • CXR
    • CT
126
Q

What are the 4 causes for non-cardiogenic edema?

A

High altitude pulmonary edema

Re-expansion pulmonary edema

Neurogenic pulmonary edema

Negative pressure pulmonary edema

127
Q

What is High altitude pulmonary edema

A

A marked rise in pulmonary artery pressure at high altitude causes fluid to leak into the interstitium

128
Q

What is Re-expansion pulmonary edema?

A

Overly rapid re-expansion of a collapsed lung during drainage of a pneumothorax or pleural effusion may lead to primarily ipsilateral edema formation

129
Q

What is Neurogenic pulmonary edema?

A

Following severe CNS injury, large rises in sympathetic outflow increases capillary hydrostatic pressure and permeability

130
Q

What is Negative pressure pulmonary edema

A

Following resolution of acute upper airway obstruction due to high negative intrathoracic pressures generated while the airway was still obstructed

131
Q

Where is pleural fluid created? How is it absorbed?

A

Pleural fluid is formed predominantly by the intercostal arteries in the parietal pleura and to a lesser extent the bronchial arteries in the visceral pleura. This fluid is then absorbed predominantly by lymphatics in the parietal pleura

132
Q

What are the 4 causes of pleural effusion?

A

Increased systemic or pulmonary capillary hydrostatic pressure

Decreased colloid osmotic pressure

Increased pleural capillary permeability

Lymphatic obstruction

133
Q

How does a pleural effusion present on CXR?

A

positive silhouette sign

blunted costophrenic angles

meniscus sign

134
Q

What are the 2 types of effusions?

A

Transudative and exudative

135
Q

What are transudative effusions? Exudative?

A

Transudative effusions

Collections of fluid that accumulate passively as the result of increased hydrostatic pressure or decreased colloid osmotic pressure

Exudative effusions

Collections of fluid caused by inflammation, increased capillary permeability, or lymphatic obstruction

136
Q

When analyzing pleural fluid studies, what criteria must be met for it to be an exudative effusion?

A

If ANY of these criteria are met, the effusion is exudative:

Pleural fluid LDH > ⅔ the upper limit of normal for the serum LDH

Pleural fluid LDH:Serum LDH is > 0.6

Pleural fluid protein:Serum protein is > 0.5

137
Q

What is a tension pneumothorax?

A

Creation of a one-way valve that fills the thoracic cavity with each inspiratory breath, but leaves no way for air to escape on exhalation → deviation of mediastinal structures and possible compression of the IVC or SVC

138
Q

What is a pneumothorax?

A

abnormal collection of air in the pleural space that causes an uncoupling of the lung from the chest wall

139
Q

What are the clinical symptoms of pneumothorax and tension pneumothorax?

A

Non-traumatic pneumothorax

  • Dyspnea
  • Chest pain
  • Hyperresonance to percussion
  • Diminished breath sounds

Tension pneumothorax

  • Tachycardia
  • Hypotension
  • Elevated JVP
  • Hyperresonance to percussion
140
Q

How does a tension penumothorax and a pneumothorax present on CXR?

A
141
Q

Define maximum oxygen uptake (VO2 max)

A

the amount of oxygen being used at peak exercise

142
Q

What are the 6 factors that determine maximum oxygen uptake?

A

Ventilation to deliver oxygen to alveoli

Gas exchange to move oxygen from the alveoli to the blood

Oxygen carriage by hemoglobin

Cardiac output to deliver oxygenated blood to the tissues

Oxygen delivery to the muscle mitochondria to generate ATP

Muscle contraction to perform the sustained exercise

143
Q

Descriebe the role of cardiopulmonary testing (CPET).

A

In this test, patients exercise on a treadmill or a bicycle. As the exercise progresses, the speed and the incline, or wheel resistance, is increased until the patient can no longer continue. During exercise, the patient’s heart rate, oxygen saturation, and ECG are continuously monitored and blood pressure is measured intermittently. In addition, the patient wears a tight fitting mask to allow collection of all exhaled gases to measure minute ventilation, oxygen uptake, and carbon dioxide production. In some cases, blood gases are measured to determine the efficiency of gas exchange and measure dead space

144
Q

Name 4 of the uses of CPET?

A

Determine a patient’s fitness to undergo a lung resection

Follow disease progression

Make treatment decisions (like when to list a HF patient for transplant)

Monitor training progress in athletes

145
Q

How does maximum exercise affect oxygen uptake?

A

Oxygen uptake increases linearly until a plateau is reached. This is due to mechanical limitations, a ventilatory threshold.

146
Q

How does maximum exercise affect cardiac output?

A

Cardiac output increases linearly until a plateau is reached. This is due to mechanical limitations (how fast can the heart beat. The faster it beats, the less time there is to fill the heart. How long increased heart rate be sustained. etc.)

147
Q

How does maximum exercise affect stroke volume?

A

Stroke volume greatly increases at the onset of exercise due to increased venous return. After that, stroke volume only increases only a little from increased inotropic activity

148
Q

How does maximum exercise affect systemic blood pressure?

A

Systemic blood pressure progressively increases with exercise. The decreased resistance in exercising muscles is counteracted by the increase in resistance from the renal, splanchnic, and skin beds

149
Q

How does maximum exercise affect pulmonary artery pressure?

A

Pulmonary artery pressure modestly increases with maximal exercise because recruitment and distention decreases PVR

150
Q

What is the ventilatory threshold?

A

the ventilatory threshold identifies a level of exertion where blood flow to the exercising muscle is no longer able to completely meet the metabolic demands.

151
Q

Does the ventilatory threshold have a temporal relationship to the lactate threshold?

A

yes

152
Q

How does maximum exercise affect CO2 tensions? (PACO2 and PaCO2)

A

PACO2 and PaCO2 both remain pretty constant in early exercise cuz alveolar ventilation increases in proportion to the increased CO2 production

Once ventilatory threshold is hit (along w/ lactic acidosis), alveolar ventilation increases a ton and both PACO2 and PaCO2 drop (compensatory respiratory alkalosis)

153
Q

How does maximum exercise affect O2 tensions?

A

PaO2 is relatively constant during exercise

PaO2 does NOT increase after ventilatory threshold, even though minute ventilation and PAO2 have increased (increased A-a O2 difference)

154
Q

How does maximum exercise affect pH?

A

Arterial pH remains constant until ventilatory threshold, then drops because minute ventilation can’t keep up with the metabolic (lactic) acidosis

155
Q

How does maximum exercise affect VD/VT?

A

because dead space is largely constant, as VT increases, the VD/VT fraction decreases

156
Q

How does maximum exercise affect the respiratory exchange ratio?

R = VCO2/VO2

VA = PIO2 x FIO2 - (PCO2/R)

A

For the purpose of this class, the value of R is 0.8. At exercise, the use of carbohydrates increases, which increases CO2 production. As CO2 increases, so does R

R can rise to levels as high as 1.1 to 1.3

157
Q

What is cardiac limitation? How do CPET data compare to individuals without cardiac limitation?

A

Cardiac limitation occurs when exercise is limited by the amount of oxygenated blood that can be delivered to the muscles. In other words, the heart reaches limitations before ventilatory or pulmonary systems fail

158
Q

What is ventilatory limitation? How do CPET data compare to individuals without ventilatory limitation?

A

Ventilatory limitation is when the respiratory system reaches its limits of its ventilatory capacity well before the heart or pulmonary vascular system

159
Q

What is pulmonary vascular limitation? How do CPET data compare to individuals without pulmonary vascular limitation?

A

pulmonary vascular limitation is inability to recruit and distend underutilized pulmonary vessels in response to increased pulmonary blood flow during exercise

CPR (27 decks)

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