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110 Cards in this Set

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Volume of air that can be expired with maximal effort after maximal inspiration
Forced vital capacity
Volume of gas expired during 1st second
FEV1
OBSTRUCTIVE DISEASE:

TLC ?
RV?
FRC?
FVC?
FEV1?
FEV1/FVC?

What is most diagnostic change?
TLC +
RV ++
FRC ++
FVC no change or -
FEV 1 --
FEV1/FVC --

Most diagnostic - decreased FEV1/FVC with increase in TLC
RESTRICTIVE DISEASE:

TLC?
RV?
FRC?
FVC?
FEV1?
FEV1/FVC?

Most diagnostic?
TLC --
RV -
FRC -
FVC --
FEV1 -
FEV1/FVC no change or increased

Most diagnostic decrease of FVC with decrease in TLC
FEV1/FVC = 80% - normal, restrictive or obstructive
Normal
FEV1/FVC = 50% - normal restrictive or obstructive
Obstructive
FEV1/FVC = 88% - normal restrictive or obstructive
Restrictive
Airway resistance is increased and expiration is impaired - all measures of expiration are decreased - FVC, FEV1, FEV1/FVC, air is trapped so increased FRC

What disease
Obstructive - ASTHMA
Increased compliance, expiration is impaired, air is trapped - increased FRC

What disease?
COPD - obstructive
Impaired alveolar ventilation - severe hypoxemia with cyanosis and increased PCO2 - blue and edematous from R heart failure
Blue bloaters --> Chronic bronchitis
Alveolar ventilation is maintained so they have normal PCO2 and only mild hypoxemia, they have reddish complexion and breathe with pursed lips at increased respiratory rate
Pink puffers --> emphysema
There is decreased compliance and inspiration is impaired - all lung volumes are decreased but because FEV1 decreases less than FVC, FEV1/FVC may be increased or normal
Restrictive pattern --> fibrosis
Daltons law of partial pressures
Partial pressure = total pressure * fractional gas concentration
Alveolar gas equation
PAO2 = PIO2 - PCO2/R
Alveolar ventillation equation
Alveolar ventilation = (Vt-Vd) * F
Ficks Law of diffusion

What changes in disease
Vgas = D (P1-P2) * A/T

A and T are physical factors that change mainly in disease
Diffusion constant of CO2 is bigger or smaller than of O2
CO2 bigger than O2
RBC remians in capillary for _ seconds

Equilibrium is reached in _ seconds in normal lung at resting state

_ reduces equilibration time but there is still enough reserve for full equillibration of oxygen in healthy individual
0.75

0.25

Exercise
Gases that EQUILIBRATE between alveolar gas and pulmonary capillaries are _

The amount of gas transferred is dependent on properties of blood gas barrier?

Examples of those gases
PERFUSION LIMITED

NO

O2 - under normal conditions

N2O

CO2
Gases that DO NOT EQUILIBRATE between alveolar gas and pulmonary capillaries are _

The amount of gas transferred is dependent on properties of blood gas barrier?

Give examples of those gases
DIFFUSION LIMITED

YES

O2 - abnormally

CO
Why is CO a diffusion limited gas
Binds so avidly to hemoglobin, PaCO doesnt increase too much - used to measure PULMONARY DIFFUSION CAPACITY
Name conditions under which O2 becomes diffusion limited gas
- Blood gas barrier is thickened in FIBROSIS

- Surface area is decreased in EMPHYSEMA

- INTENSE EXERCISE decreases time for equilibration in pulmonary capillaries (can occur in normal lungs)

- LOW O2 GAS MIXTURE (less partial pressure gradient, can occur in normal lungs)
Each Hb molecule has _ subunits

Each subunit has _ moiety with iron in ferrous state (Fe2+) and two _ and two _ polypeptide chains
4

Heme, alpha and beta
Maximal amount of O2 that can bind to Hb
O2 capacity
Total O2 in blood (bound + dissolved)
O2 content
_ reflects O2 bound to Hb (the amount of O2 that is dissolved is trivial compared to bound)
CONTENT
_ reflects dissolved O2
Partial pressure
Normal Pa O2

Normal PvO2

Normal P50
100

40

27
At Pa O2 (100 mm Hg) saturation is _

At PvO2, saturation is _

At P50, saturation is _
Almost 100%

75%

50%
Shift of Hb curve to the right - what causes it, what does it mean, what else shifts to the right
FACILITATES UNLOADING IN TISSUES

Increased temperature, PCO2, 2,3- DPG and decreased pH

P50 also shifts to the right

*** Exercising muscle is hot, acidic and hypercarbic
Shift of Hb curve to the left - what causes it, what does it mean, what else shifts to the left
FACILITATES LOADING OF OXYGEN

Decreased temperature, PCO2 and DPG and increased pH

P50 decreased - shifts to left

**** CO poisoning
Polycythemia and anemia change _

What stays the same
Arterial O2 content

PaO2 and P50
CO poisoning is dangerous for 3 reasons - name them
CO LEFT SHIFTS the curve, decreasing P50 causing decreased oxygen unloading in tissues

CO has 240 times greater affinity for Hb as O2 so it DECREASES OXYGEN CONTENT OF BLOOD

CO inhibits cytochrome oxidase
Forms of CO2
HCO3 = 90%

Carbamino compounds (combination of CO2 with proteins especially Hb) = 5%

Dissolved CO2 = 3%
Resistance of pulmonary blood flow - high or low
Very low
Compliance of pulmonary blood flow - high or low
Very high
Pressure in pulmonary circulation
Very low compared with systemic circulation
Effect of lower PaO2 on pulmonary blood flow
ALVEOLAR HYPOXIA CAUSES VASOCONSTRICTION

This is a local effect and the opposite of other organs where hypoxia causes vasodilation

This directs blood away from hypoxic alveoli to better ventilated areas

This is also why fetal pulmonary vascular resistance is so high - pulmonary resistance decreases when the first breath oxygenates alveoli causing pulmonary blood flow to rise
In upright posture due to effect of gravity, flow is greatest in _ and lowest in _
Base

Apex
What metabolic changes take place in lungs
Conversion of angiotensin I to angiotensin II, inactivation of bradykinin, remove prostaglandins E2 and F2alpha and leukotrienes
BLOOD FLOW is highest at _ and lowest at _

VENTILATION is higher at _ and lowest at _

The change in ventilation is not as great as blood flow so V/Q RATIO is higher at _ and lowest at _
BASE = HIGH
APEX = LOW

BASE = HIGH
APEX = LOW

BASE = LOW
APEX = HIGH
If ventilation is 0 (airways blocked), V/Q = _ which means patient has a _ --> no gas exchange occurs and PAO2 and PCO2 are the same as _
V/Q = 0

Shunt

Mixed venous blood (O2 = 40, CO2 = 45)
If perfusion is 0, patient has _ , V/Q ratio = , no gas exchange occurs and PAO2 and PACO2 are the same as _
Pulmonary embolism

V/Q = infinity - dead space

Inspired air (O2 = 150, CO2 = 0)
Where is higher?

Ventilation

Perfusion

V/Q

PO2

PCO2
Base

Base

Apex

Apex

Base
In hypoventilation what happens to

PaO2

PaCO2

CaO2

Aa gradient

Response to supplemental O2
Decreased

Increased

Decreased

Not changed

Responds to O2 by increase in PaO2 and CaO2
Decrease in inspired PO2 (high altitude)

What happens to

PaO2

PaCO2

CaO2

Aa gradient

Response to supplemental O2
Decreased

Decreased

Decreased

Not changed

Responds to supplemental O2 by increase in PaO2 and CaO2
Diffusion limitation (PAO2 and PaO2 do not fully equilibrate)

What happens to

PaO2

PaCO2

CaO2

Aa gradient

Response to supplemental O2
Decreased

Not changed

Decreased

Increased

Respond to supplemental O2 by increase in PaO2 and CaO2
Shunt (venous blood mixes with arterial bypassing ventilated areas of the lung)

What happens to

PaO2

PaCO2

CaO2

Aa gradient

Response to supplemental O2
Decreased

Not changed

Decreased

Increased

Poor response to O2
V/Q mismatch

What happens to

PaO2

PaCO2

CaO2

Aa gradient

Response to supplemental O2
Decreased

Not changed

Decreased

Increased

Responds to O2 by increasing PaO2 and Ca O2
CO poisoning (exhaust fumes)

What happens to

PaO2

PaCO2

CaO2

Aa gradient

Response to supplemental O2
Not changed

Not changed

Decreased

Not changed

O2 results in increase of PaO2 but no changed in CaO2 (increased affinity of CO for Hb)
Decreased Hb (anemia)

What happens to

PaO2

PaCO2

CaO2

Aa gradient

Response to supplemental O2
Not changed

Not changed

Decreased

Not changed

Increase in PaO2 but not in Cao2
Generates breathing rhythm
Inspiratory center in medulla
Not active during normal passive expiration involved in active expiration (exercise)
EXPIRATORY CENTER in medulla
Stimulates prolonged inspiration
Apneustic center in pons
Trminates inspiration
Pneumotaxic center in ponse
Lesions above ponse eliminate _ but _ remains intact
Voluntary control

Basic breathing pattern
Central (medulla) chemoreceptors respond to _

Reaction to O2

Reaction to CO2

Reaction to H+
Changes in pH of CSF

No response

INCREASED PCO2 --> stimulate chemoreceptors --> INCREASED VENTILATION (via H+)

Increased H+ --> stimulation of increased ventilation detects H+ in CSF, 80-95% response to hypercapnia
Peripheral cehmoreceptors (carotid and aortic bodies)

Response to O2

Response to CO2

Response to H+
Decreased PaO2 --> stimulates chemoreceptors --> increased ventilation

***Stimulated by changes in pressure not O2 content so wouldnt respond to anemia

Increased PCO2 --> stimulation - increased ventilation but central chemoreceptor response is most important during normal breathing

Increased H+ --> stimulation --> increased ventilation

*** Most of the response to metabolic acidosis is peripheral because fixed acids penetrate blood brain barrier poorly
Patients with severe lung disease can have chronic CO2 retention and _ can return to normal despite their hypercapnia

Having lose their CO2 stimulus to ventilate their _ becomes very important

Therefore you shouldnt give those patients _ because _
pH of CSF

Hypoxic ventillatory drive (peripheral chemoreceptors)

Enriched O2 to breathe because primary ventillatory drive will be removed which cause severe depression of ventillation
RESPONSE TO HIGH ALTITUDE

PAO2

PaO2

Respiratory rate

Pa and PA CO2

Arterial pH

Hb

HB % saturation

Pulmonary vascular resistance

2,3 DPG

HbO2 curve


What problems can occur?
PAO2 --> decreased because of decrease in barometric pressure

PaO2 --> decreased because of hypoxemia caused by decrease in PAO2

Respiratory rate --> increased --> hypoxia stimulates peripheral receptors

PaCO2 and PACO2 --> increased because of hyperventilation due to hypoxemia

Arterial pH --> increased because of respiratory alkalosis, later becomes normal due to renal compensation

Hb --> increased = polycythemia

Hb saturation ---> decreased because of decreased PO2

PVR --> increased due to hypoxic vasoconstriction, this plus polycythemia lead to increased work and hypertrophy of R heart

2,3 DPG --> increased

Hb-O2 curve --> shifts to right (because of increased 2,3 DPG)

Also 2 problems:

Acute mountain sickness - hypoxemia and alkalosis cause headache, fatigue, nausea, dizziness, palpitations and insomnia, treat with acetozalomide

Chronic mountain sickness causes reduced exercise tolerance, fatigue, hypoxemia and polycythemia
Increased resistance to airflow secondary to obstruction of airways - what disease
COPD
COPD includes _
Chronic bronchitis

Emphysema

Asthma

Bronchiectasis
Persistent cough and copious SPUTUM PRODUCTION FOR AT LEAST 3 MONTHS each year in 2 consecutive years, highly ASSOCIATED WITH SMOKING (90%)
CHRONIC BRONCHITIS
Patient presents with cough, sputum production, dyspnea, frequent infections, PE shows hypoxia, cyanosis and weight gain
Chronic bronchitis
Associated with destruction of alveolar speta, resulting in enlarged air spaces and loss of elastic recoil and producing overinflated enlarged lungs, thought to be due to protease/antiprotease imbalance
Emphysema
Autopsy shows OVERINFLATED, ENLARGED LUNGS, enlarged grossly visible air spaces and formation of apical blens and bullae (which type? )
Emphysema

Centriacinar type
Patient presents with progressive dyspnea, he uses pursing of lips and ACCESSORY MUSCLE to breathe. PE shows BARREL CHEST and weight loss
Emphysema
Centriacinar (centrilobular) emphysema

Which part of bronchioles involved

Associated with ?

Worst in _
PROXIMAL RESPIRATORY BRONCHIOLES

SMOKING

Worst in apical segments of upper lobes
What is the most common type of emphysema (95%)
Centriacinar (centrilobular)
Panacinar (panlobular) emphysema

- Which part involved?

_ Associated with?

- Distribution?
ENTIRE ACINUS INVOLVED, distal alveoli spared

ALPHA 1 ANTITRYPSIN DEFFICIENCY

Distribution - whole lung, worse in bases of lower lobes
- Due to hyperreactive airways resulting in episodic BRONCHOSPASM, producing WHEEZING, severe DYSPNEA and coughing
Asthma
Biopsy of the lung shows inflammation, edema, hypertrophy of mucous glands with GOBLET CELL HYPERPLASIA AND MUCUS PLUGS, also hypertrophy of bronchial wall smooth muscle and thickened basement membranes
ASTHMA
Exrinsic asthma

Mechanism

What type is most common

Who usually gets it

What triggers it
TYPE I HYPERSENSITIVITY reaction

ALLERGIC (ATOPIC) - most common type

Childhood and young adults, especially with POSITIVE FAMILY HISTORY

Allergens - pollen, dust, food, molds, animals, occupational exposure
Intrinsic asthma

Possibel triggers
RESPIRATORY INFECTIONS (usually viral)

STRESS

EXERCISE

COLD temperatures

Drug induced - ASPIRIN
Bronchiectasis - an abnormal permanent airway dilation due to _

Who usually gets it?
CHRONIC NECROTIZING INFECTION

Most patients have underlying lung disease such as bronchial obstruction, necrotizing pneumonias, CYSTIC FIBROSIS or KARTAGENER SYNDROME
Give examples of restrictive lung disease
CHEST WALL DISORDERS- obesity, kyphoskoliosis, polio

INTRINSIC LUNG DISEASE - ARDS, NRDS, pneumoconioses, sarcoidosis, fibrosis, Goodpastures and WG syndrome, eosinophillic granulomas, collagen vascular disorders, hypersenstivity pneumonias, drug exposure
Diffuse damage to alveolar epithelium and capillaries resulting in progressive respiratory failure unresponsive to oxygen therapy
ARDS
What are the possible causes of ARDS
Shock, sepsis, trauma, gastric aspiration, radiation, oxygen toxicity, drugs, pulmonary infections, etc
Patient presents with dyspnea, tachypnea, hypoxemia and cyanosis and is using accessory respiratory muscles, x ray shows BILATERAL LUNG OPACITY ("white out"). Patient dies and autopsy shows heavy STIFF NON COMPLIANT LUNGS, interstitial and intra alveolar edema, interstitial inflammation, loss of type I pneumocytes and HYALINE MEMBRANE FORMATION
ARDS
Causes respiratory distress wihin hours after birth and seen in infants with _ secondary to prematurity, maternal diabetes, multuple births or C section - diagnossi
Defficiency of surfactant

NRDS
Baby girl was born at 26 weeks, was normal at birth but within few hours developed increasing respiratory effort, tachypnea, nasal flaring, use of accessory muscles of respiration, expiratory grunt and cyanosis, x ray shows GROUND GLASS reticulogranular densities, labs show lecithin:sphingomyelin ratio of 1.5. Lung biopsy shows atelectasis and HYALINE MEMBRANE FORMATION

Diagnosis
Treatment
Prevention
Diagnosis- NRDS

Treatment -surfactant replacement and oxygen

Complications of oxygen treatment - BRONCHOPULMONARY DYSPLASIA AND RETROLENTAL FIBROPLASIA (retinopathy in newborns)

Prevention- delay labor and corticosteroids to mature the lung
Pulmonary edema common causes
L sided heart failure
MV stenosis
fluid overload
nephrotic syndrome
liver disease
infections
drugs
shock
radiation
Pulmonary emboli mostly rise from _ and may be asymptomatic, cause pulmonary infarction or cause sudden death - severity related to size of embolus and other comorbid conditions
DEEP VEIN THROMBOSIS in the leg (also arise from pelvic veins)
_ forms in the ventral wall of foregut
Respiratory (laryngotracheal) diverticulum
Divides foregut into esophagus and trachea
Tracheoesophageal septum
Abnormal communication between trachea and esophagus caused by malformation of tracheoesophageal septum

90% occur between esophagus and _

Generally associated with what conditions?

Symptoms?
Tracheoesophageal fistula

Distal 1/3 of trachea

Esophageal atresia and polyhydramnios

Gagging and cyanosis after feeding and reflux of gastric contents into lungs causing pneumonitis
Terminal bronchioles divide into _ which contain alveoli and branch to form alveolar ducts, ducts terminate in _ and are lined by _
RESPIRATORY BRONCHIOLES

alveolar sacs

Squamous alveolar epithelium
Thin walled sacs responsible for gas exchange
Alveoli
Provide thin surface for gas exchange
Type I pneumocytes
Produce SURFACTANT
Type II pneumocytes
Nasopharynx communicates with nasal cavity through _
Choanae
Abducts vocal folds
Posterior cricoarytenoid
Adducts vocal fold
Lateral cricoarytenoid
Tenses vocal fold
Cricothyroid
Relaxes vocal fold
Thyroarytenoid (including vocalis)
Opens laryngeal inlet
Thyroepiglotticus
Closes laryngeal inlet
Aryepiglotticus
Oblique and transverse arytenoids
The only laryngeal muscle that is innervated by external laryngeal nerve - branch of superior laryngeal branch of vagus

All other intrinsic muscles of larynx are innervated by _
Cricothyroid

Recurrent laryngeal nerve
Divided by oblique and horizontal fissures into three lobes
Right lung
Has only one fissure - oblique
Left lung
Superficial drainage of lungs is to _ nodes from there to _

Deep drainage to _ from there to _

Bronchomediastinal lymph trunks drain to the _
Bronchopulmonary - tracheobronchial

Pulmonary - bronchopulmonary

Right lymphatic and thoracic ducts
Air inspired and expired in normal breathing
Tidal volume
Volume in lungs with maximal inspiration
Total lung capacity
Volume in lungs at end of quiet passive expiration, the equilibrium point of the system
FRC
Volume at the end of maximal forced expiration
Residual volume
Volume expired from maximal inspiration to maximal expiration
Vital capacity
The volume inspired with maximal inspiratory effort in excess of tidal volume
IRV
The volume expelled with active respiratory effort after passive expiration
ERV
The volume of air inspired with maximal inspiratory effort after passive expiration
Inspiratory capacity
Cannot be measured with spirometry
FRC
RV