EXAM 4 MODULE 10 PATHO (copy)

where does gas exchange occur?

what 3 things need to happen at the same time?

what problems can occur if there are issues with those 3 things?

alveolar-capillary membrane

ventilation, perfusion, diffusion

hypoxemia or hypercarbia (high arterial CO2 concentration)

ventilation

process of moving air into the lungs and distributing air within them to alveoli to maintain O2 and remove CO2

tidal volume

normal breathing (500 mL)

inspiratory volume

amount of gas one can inhale to the max (3L)

expiratory volume

amount of gas one can exhale to the max (1.2L)

residual volume

volume of gas left in lungs after a max exhalation (1.2L)

vital capacity

total amount of gas exhaled during a max exhalation (4.8L)
taking a deep breath in and then a complete breath out (how much you breathe out)

inspiratory capacity

total amount of gas inhaled during an inhalation and resting expiration (3.5L)
take a deep breath in and hold it

functional residual capacity

amount of gas left in the lungs after a normal exhalation (2.4L)

total lung capacity

amount of gas contained in the lungs at maximal inspiration (6.0L)

dead space

physiologic

anatomic

alveolar

1/3 area of lungs that doesn't do gas exchange

phy: anatomic + alveolar dead space

ana: volume of gas (not in exchange) in the airways from nose to resp bronchioles, 1mL per pound of weight (150mL)

alv: ventilated, unperfused alveoli (wasted ventilation)

minute ventilation

someone with a tidal volume of 500 mL breathing @ 15bpm has what min ventilation?

tital volume x RR

7500 mL

alveolar ventilation equation

difference of tidal volume and anatomic dead space x RR

what does slow deep breathing yield?

greater alveolar ventilation

what is PAo2?

the partial pressure of oxygen in alveoli, driving force to move O2 into blood

Law of 5's

how to calculate expected PAo2
multiple FIO2 by 5
estimates what O2 level should be under normal health conditions

mechanisms of breathing

airway resistance
lung compliance
opposing forces (elastic recoil vs chest wall expansion)

airway resistance
what is it influenced by?

relationship between driving pressure and flow
driving pressure + rate of airflow
influenced by airway radius and pattern of gas flow, stress, age

lung compliance
equation?

lung expandability, ease of lung inflation
change in volume/change in pressure

opposing lung forces
expiration and inspiration

mechanic of breathing
elastic recoil vs chest wall expansion
exp: lungs recoil, chest wall moves in, diaphragm moves up
ins: lungs expand, chest wall moves out, diaphragm moves down

what increases and decreases lung compliance?

inc: destruction of elastic fibers (age, obstructive disease)
dec: excessive fiber production

what can decrease chest wall distensibility and decrease
compliance?

obesity, abdominal distention, pregnancy, kyphoscoliosis, abnormal surgery

airway resistance
what does resistance do as radius of airway tube decrease?
equation?
what does parasypm stim result in?
what does symp stim result in?

determined by relationship between driving pressure and flow
increase
driving pressure/rate of air flow
constriction
dilation

laminar flow
turbulent flow
transitional flow

small airways, minimal resistance
nasal cavity to large bronchi, friction, increase resistance
larger airways, at bifurcations

distribution of ventilation
upright
supine

up: ventilation greatest near bottom of lung and decreases toward apex, alveoli are larger in apex
sup: ventilation best in dependent part of lung field (lowest part)

neurologic control of ventilation
neural control centers?

chemoreceptors?

what does the Herin-Breur reflex prevent?

what do proprioceptors in muscles and tendons respond to?

what do baroreceptors in aortic and carotid arts respond to?

medulla oblongata and pons

central ones respond to CO2 and pH changes

peripheral ones respond to decreases in arterial O2

overinflation of the lung

body movement

changes in blood pressure

how much blood in the lungs at any time?

450 mL or 9% of total amount

how is blood flow affected?
zone 1 distribution of blood flow
zone 2
zone 3

uneven, affected by body position
1: no perfusion, like dead space
2: intermittently perfused
3: continuously perfused

ventilation-perfusion ratios

4L/min of alveolar ventilation to 5L/min capillary blood flow

what can abnormalities of VA/Q matching result in?

inadequate oxygenation of blood and insufficient CO2 removal

hypoxic vasoconstriction

vessels in lung that are poorly ventilated, constrict to minimize imbalances, divert blood to better ventilated areas

the zones of the lung are characterized by differences in?

blood flow or perfusion

6 barriers of alveolar-capillary membranes

surfactant
alveolar membrane
interstitial fluid
capillary membrane
plasma
RBC membrane

what is oxygen concentration in alveoli, and partial pressure controlled by?

rate of absorption in blood
rate of entry of new O2 into lungs by ventilation process

what are the 2 forms of oxygen transport?

dissolved in solution, bound to hemoglobin

oxyhemoglobin saturation curve def
when is hemoglobin fully saturated?

does an increase in PaO2 to more than 100 improve O2 content?

describes relationship with PaO2 and hemoglobin saturation
at a PaO2 of 90-100mmHg

no it does not

shift to left in oxyhemo curve

shift to right

(loading in lungs) increased affinity for hemoglobin in the lungs, dec H+ concentration, inc pH, dec PCO2, dec temp, dec 2,3 DPG, alkalotic

decreased affinity, enhances unloading of CO2, acidic, inc H+ concentration, dec pH, inc PCO2, inc temp, inc 2,3 DPG

how is CO2 transported?

dissolved in plasma
through carbaminohemoglobin
bicarbonate iron

bicarbonate ion

formed from CO2 + H20
then dissociates into HCO3- and H+
then CO2 formed, diffuses into alveoli

when does ventilatory failure occur?

what does this result from?

when does ineffective gas exchange occur?

when alveolar ventilation is insufficient to accomplish adequate gas exchange

decreased resp rate, decreased tidal volume, inc dead space

an adequate volume of gas is maldistributed, minute ventilation dec, and/or alveolar hypoventilation happens

hypoxic hypoxia

anemic hypoxia

circulatory hypoxia

histotoxic hypoxia

PaO2 is dec even though there is normal O2-carrying capacity (high altitude, hypoventilation)

decreased O2-carrying capacity (decrease Hgb)

low cardiac output where O2-cc is normal but blood flow is reduced (shock, CHF)

interference of a toxic substance leads to inability of tissues to utilize avaliable O2 (cyanide posioning)

Low VA/Q

low ventilation, high perfusion
alveolar hypoxia
high Pco2, low Po2

High Va/Q
what is major cause of this?

high ventilation, low perfusion
pulmonary embolism
low Pco2 and high Po2

Shunt areas

no ventilation, well perfused (blood flow passes unventilated alveoli)
blood goes from R --> L with NO gas exchange

acute respiratory failure
what causes it?

what pathophysiologic mechanisms

depend on cause?

clinical manifestations?

diagnosis

treatment

hypoventilation, ventilation-perfusion mismatch, R-L shunt
drugs, chest wall deformities, trauma

CNS, neuromuscular disease, chest wall and diaphragm, airway, pulmonary parenchymal disease

confusion, tremors, hypotension, depressed consciousness, tachypnea, tachycardia

ABO (PaO2 of less than 60, PaCO2 greater than 50), chest radiography, pH of less than 7.3

maintain ventilatory support by maintaining airway patency, ensuring adequate alveolar ventilation
mechanical ventilation, supportive care

forced vital capacity

normal L

obstructive L

restrictive L

total volume of air exhaled
max volume of air you exhale out with a max exhalation

4.0L

4.0L

3.0L

forced expiratory volume in 1 second (FEV1)

normal L

obstructive L

restrictive L

forced expiratory volume in 1 second
deep inhale/exhale as fast as you can in 1 second

3.0L

1.0L

2.5L

FEV1/FVC ratio
no sig obstruction
mild obstruction
mod obstruction
severe obstruction

forced vital capacity/FEV1 (reliable index of obstructive)
more than 75%
60-70%
50-60%
less than 50%

diff types of pulmonary function testing

spirometry
diffusion capacity (total lung capacity)
arterial blood gases
bronchial provocation testing (controlled induction of bronchospasm by inhalation of agents)

pulmonary function testing abnormalities

decreased FEV1
low FEV1/FVC ration (less than 70%)
improvement in FEV1 after bronchodilator in asthma
increased reisdual volume and residual capacity

pulmonary hypertension etiology

types

sustained increase in pulmonary artery pressure about 25mmHg systolic resting, above 30 systolic in exercise

primary pulmonary hypertension (idiopathic), more common in women
secondary pulmonary hypertension from known disease process (increased left atrial pressure, inc pulm blood flow)

pathogenesis (what happens in body?) of pulmonary hypertension

what can it lead to?

small pulmonary vessels thicken
internal layer of pulm artery wall becomes fibrotic
muscle development occurs in vessels normally nonmuscular, plexiform lesions form
tissue necrosis and hemorrhage
vasoconstriction, obstruction

can lead to right sided heart failure

clinical manifestations of pulmonary hypertension

diagnosis

treatment

what are advanced stages of PPH?

exercise intolerance, syncope, dyspnea, chest pain on exertion, fatigue, pulmonary edema, hemoptysis
right sided heart failure and right ventricular hypertrophy

pulm artery catheter, chest radiograph, 12-lead ECG, echocardiogram

early ID and control of disease
lung or heart-lung transplant
long-term infusion of prostacyclin

irreversible

pulmonary venous thromboembolism etiology

pathogenesis

what is the most common cause? and where/how do they form?

what does impact depend on?

undissolved detached material that occludes blood vessels of pulmonary vasculature

once blood clots released to venous system, they travel to pulm vasculature
emboli may be composed of fat, air, amniotic fluid, thrombi

thrombi, forms in leg under conditions of venous stasis, hypercoagulability, endothelial injury

size and cross-sectional area of circulatory impariment

clinical manifestations of PVT

diagnosis

treatment
treatment for suspected or confirmed PE

what to treat with if patient is releasing multiple emboli despite heparin therapy?

treatment in emergency?

depends on size of embolus, PE suspected with dyspnea and chest pain suddenly

high VA/Q
helical angiography
pulmonary arteriography
duplex ultrasonography of lower extremities

prevention (anticoagulants)
supplemental O2 or ventilator
activity limitations
continuous heparin IV drip
thrombolytic therapy

umbrella filter (mobin-uddin) or "bird's nest" filter

embolectomy

disorders with obstruction from conditions in the wall of the lumen

asthma
acute bronchitis
chronic bronchitis

disorders with obstruction related to loss of lung parenchyma

emphysema

disorders with obstruction of the airway lumen

bronchiectasis, bronchiolitis, cystic fibrosis, epiglottis, acute tracheobronchial obstruction, croup

restrictive disorders with lung parenchyma disorders

fibrotic interstitial lung diseases

types of fibrotic interstitial lung diseases

diffuse interstitial lung disease
sarcoidosis
hypersensitivity pneumonitis
occupational lung diseases

restrictive disorders with pleural space disorders

pneumothorax
pleural effusion

restrictive neuromuscular, chest wall, obesity disorders

poliomyelitis, amyotrophic lateral sclerosis, muscular dystrophies, guillain-barre syndrome, myasthenia gravis

kyphoscoliosis, ankylosing spondylitis, flail chest

obesity

restrictive disorders with infection or inflammation of the lung

pneumonia
severe acute resp syndrome
middle east resp syndrome
COVID
pulmonary tuberculosis

obstructive disorders

classifications

manifested by increased resistance to airflow

obstruction from conditions in wall of lumen (asthma, bronchitis)
obstruction from inc pressure around outside of airway lumen (emphysema)
obstruction of airway lumen (cystic fibrosis, acute tracheobronchial obstruction)

asthma etiology
phenotypes
types

pathogenesis

how does inflammation contribute?

strongest predisposing factors?

airway obstruction, reversible, airway inflammation
increased airway reactivity to a variety of stimuli
early-onset, late-onset eosinophilic, exercise-induced, obesity-related, neutrophilic
non-allergic, adult onset (intrinsic)
allergic, ped onset (extrinsic)

denudation of airway epithelium
collagen deposition beneath basement membrane
edema, mast cell activation
inflammatory cell infiltration by neutrophils, eosinophils, lymphocytes

acute bronchospasm, mucosal edema, mucous plug formation, airway wall remodeling

genetic predisposition for atopy and structural deposition

pathogenesis of extrinsic/allergic asthma

mechanism of action

clinical

severe clinical

IgE mediated (elevated levels)
allergic rhinitis
eczema, pos family history
attacks associated with seasonal, environmental, occupational exposure

initiated by exposure to a specific antigen that has previously sensitized mast cells in airway mucosa

wheezing, tightness of chest, dyspnea, cough, increased sputum

severe: use of accessory muscles, intercostal retractions, distant breath sounds with insp wheezing, orthopnea, agitation, tachypnea, tachycardia, peak expiratory flow rate of less than 80 L/min

status asthmaticus

severe form of asthma that fails to respond to typical use of inhaled bronchodilators
if wheezing stops, patient is in trouble

diagnosis of asthma

treatment

history, physical findings, sputum exam, pulm function tests, blood gas analysis, chest radiography
PEFR measured to determine index of airway function, max flow of expired air during FVC

prevention, desensitization, prophylactic drug therapy
bronchodilators, corticosteroids, o2 therapy

adrenergics
steroids
theophylline
hydration IV
mask O2
anticholinergics

pneumonia etiology

what can it result from? 3 sources

how can it be acquired?

diff types?

inflammatory reaction in alveoli and interstitium of lung, caused by an infectious agent

aspiration of oropharyngeal secretions composed of normal bacteria flora and/or gastric contents (20-35% of all pneumonia), diminished gag reflex

inhalation of contaminants (virus, mycoplasma) --> immunocompromised at risk

contamination from systemic circulation

community or hospital

bacterial, atypical, viral
gram positive or gram negative test

pneumonia patho

what does viral not produce?
what does bacterial produce?

cm

bacteria sx

viral sx

defense mechanisms compromised (community-acquired)
bacterial in origin
alveolar air spaces fill with exudative fluid (significant V/Q mismatching, poor blood gas value)

exudative fluid (clear sputum)
green and yellow sputum

age/severity of disease cause sx variations

crackles, bronchial breath sounds, chills, cough, purulent sputum, abnormal chest radiograph

upper respiratory prodrome, wheezing, rales

pneumonia diagnosis

CURB-65

chest radiograph, gram stain of sputum, blood cultures, WBC more than 15,000 acute bacterial

c: confusion (mental score of more/equal 8)
u: uremia (blood urea more than 7 mmol/L - 19 mg/dL)
r: respiratory rate (more than 30 bpm)
b: blood pressure (less than 90, less/equal to 60)
65: 65 years of age or older

pneumonia treatment

specific antibiotic selection based on sensitivity of organism to diff antibiotics

chest x-ray repeated 6-8 weeks after treating infection

where is one's oxygen saturation likely to be lowest?

where does perfusion happen continuously?

when someone is lying on their right side

happens at the bottom of the lungs

what can combined conditions of asthma and bacterial pneumonia increase the risk for developing?

hypoxemia
both lead to V/Q mismatch
poor ventilation leads to hypoxemia

common manifestations of bacterial pneumonia include all of the following except

fever
productive cough
tachypnea
hyperinflation

hyperinflation

asthma is an obstructive disease, whereas pneumonia is a restrictive one. A major difference between them is that in restrictive diseases...

lung tissue itself is not involved in the disease process
peak expiratory flow is not decreased
lung compliance is not altered
inflammatory process is not part of patho condition

peak expiratory flow is not decreased (it is decreased in obstructive)

chronic bronchitis (type B COPD) etiology

how is it diagnosed with cough?

persistent narrowing of airways, chronic inflammation, scarring, excessive mucus
poor ventilation of alveoli, impaired O2/CO2 exchange
cigarette smoking, repeated airway infections, genetic predisposition, inhalation of chem irritants, irreversible

symptomatically, productive cough lasting more than 3 months per year for 2 years

chronic bronchitis pathology

chronic inflammation/swelling of bronchial mucosa = scarring
increased fibrosis of mucous membrane
hyperplasia/hypertrophy of bronchi mucous glands/goblet cells
inc bronchial wall thickness
alveolar hypoxia = pulmonary vasoconstriction, pulm hypertension, right ventricular hypertrophy
R-HF bc of high pulm resistance

chronic bronchitis diagnosis

treatment

chest radiography
pulm function tests (inc residual, dec FEV1)
ABO (inc PaCo2, dec PaO2)
electrocardiogram (R vent hypertrophy)
polycythemia
physical examination (crackles, ronchi, wheezes, JVD, clubbing, pedal and ankle edema)

block disease progression
return patient to optimal resp function, usual activities
low-dose extra O2
lifestyle mod (stop smoking, hydrate, vaccine)
pharmacologic therapy

chronic bronchitis clinical manifestations

cyanotic
recurrent cough & inc sputum production
hypoxia
hypercapnia
resp acidosis
inc Hbg, inc RR
exertional dyspnea
inc incidence in heavy cigarette smokers
clubbing
cardiac enlargement
use of accessory muscles to breath
leads to R heart failure

emphysema (type A COPD) etiology, what causes it

destructive changes of alveolar walls and ab enlargement of distal air sacs
irreversible
associated with chronic bronchitis, follow bacterial lung infection
smoking, air pollution, welding, mining, a1-antitrypsin deficiency

emphysema patho

alveolar destruction with release of proteolytic enzymes from inflammatory cells (neutrophils, macrophages)
dec in surface area for gas exchange
airway collapse attributable to loss of radial traction (air trapping)
terminal bronchiole with narrowed lumen = loss of surrounding alveoli, leading to dec traction & collapse

emphysema clinical manifestations

inc CO2 retention (pink)
minimal cyanosis
pursed lip breathing
dyspnea
hyperresonance on chest percussion
orthopneic
barrel chest
exertional dyspnea
prolonged expiratory time
speaks in short jerky sentences, anxious
use of accessory muscles to breathe
thin appearance

emphysema diagnosis

treatment

history findings
inc functional residual capacity
RV, TLC
dec FEV1/FVC
chest radiographs
ABGs (dec PaO2, normal to low PaCO2)
electrocardiogram (sinus tachycardia, supraventricular arrhythmias)

maintain proper nutrition, pharm, o2, stop smoking, supportive therapies

what is barrel chest due to?

increased residual lung volume

what disease are those with emphysema at risk for?

cancer
pneumothorax
pleural effusion
tuberculosis

pneumothorax

people with emphysema can maintain normal ABGs until advanced because of

increased respiratory effort

with COPD (emphysema), people exert most of their work of breathing during BLANK phase of resp, while patients with restrictive diseases exert most of their breathing work during BLANK phase

expiratory
inspiratory

cystic fibrosis etiology

patho

autosomal-recessive disorder of exocrine glands
airflow obstructive disorder or as a suppurative disorder
survival age is 31 yrs

mutations in CFTR gene= alteration in chloride/water transport across apical surface of epithelial cells
affects pancreas, intestinal tract, sweat glands, lungs, infertility in male
mucus glands in GI tract enlarge, excess secretions

cystic fibrosis cm

treatment

history of cough in child, thick sputum, recurrent pulm infections, recurrent bronchitis
progress to pneumonia and bronchiectasis, RHF, exercise intolerance, abdominal distention, rectal prolapse, stinky stool
clubbing, dyspnea, tachypnea, sternal retractions, unequal breath sounds, moist basilar crackles, ronchi, barrel chest

bronchodilators
postural drainage
chest physiotherapy
forced exp technique
recombinant human DNase
antibiotic therapy
nutritional therapy
heart-lung or lung transplant

pneumothorax etiology

patho: primary
seconday
tension

accumulation of air in pleural space

rupture of small sub pleural blebs in apices of lungs, spontaneous, tall, thin men 20-40 yrs
complications from underlying lung problem
buildup of air pressure in pleural space
ipsilateral lung collapses
mediastinal shift to opposite site
decreased venous return and cardiac output
traumatic cause or illness or treatment

pneumothorax clinical manifestations

diagnosis

treatment

tachycardia, dec/absent breath sounds on affected side, hyperresonance, sudden chest pain on side, dyspnea

chest radiograph, electrocardiogram, ABG analysis

less than 15-25% collapse: treated symptomatically
more than 15-25%: chest tube w/water seal & suction, 100% O2
chemical pleurodesis, recurrent spontaneous pneumothorax (allows lung to stick so it doesn't collapse)

pleural effusion etiology

patho

cm

diagnosis

treatment

pathologic collection of fluid or pus in pleural capacity as result of another disease

trans: inc hydrostatic or dec oncotic pressure
exu: inc production of fluid, inc permeability of pleural membrane, impaired lymphatic drainage
emphysema, hemothorax or hemorrhagic, chylothorax or lymphatic

depend on cause and size of effusion

thoracentesis should be done to analyze fluid and reduce amount of pleural cavity
chest radiography, computed tomography, ultrasonography

directed at underlying cause of effusion and relief of sx

closed-chest drainage systems work to re expand a lung after pneumothorax by

reestablishing the normal negative intrapleural pressure

acute resp distress syndrome (ARDS) etiology

patho

damage to alveolar-capillary membrane

initial injury caused by direct or indirect damage (important)
noncardiogenic pulm edema with leaky pulm capillaries
atelectasis associated with lack of surfactant
fibrosis associated with inflammatory deposition of proteins

ARDS cm

history of a precipitating event that has led to a low blood volume state

tachypnea
dyspnea
retractions
hypoxia, tachycardia
dec pulmonary compliance
dec PO2
inc dyspnea
regardless of FiO2 level, patient doesn't improve

ARDS diagnosis

treatment

refractory hypoxemia (doesn't respond to inc levels of supplemental o2)
hypercarbia, hypoxemia
white lung
blood/urine cultures
dec VC, dec FRC, dec compliance, dec tidal volume, lung biopsy

therapy
treat cause, maintain fluid/electrolyte balance
mechanical ventilation with positive end-expiratory pressure and supplemental O2

Acute Respiratory Failure etiology

patho

cm

diagnosis

treatment

hypovent, vent-perfusion mismatch, right-to-left shunt may lead to resp failure (drugs, neuromusclar weakness, chest wall deformities, trauma, parenchymal lung disease)

CNS, neuromuscular disease & related disorders, chest wall/diaphragm, airway, pulm parenchymal disease

confusion, tremors, hypotension, depressed consciousness, tachypnea, tachycardia

PaO2 of less than 60 mm Hg and PaCO2 of greater than 50 mm Hg on room air
chest radiography

maintain ventilatory support by maintaining airway patency and ensuring adequate alveolar ventilation
mechanical ventilation
supportive care

diffuse interstitial lung disease

restrictive disease with thickening of alveolar interstitium

sarcoidosis

acute or chronic system disease of unknown cause, likely with immunologic basis