Final Flashcards
nasopharynx
the upper part of the throat that connects the nasal passages to the larynx and trachea
oropharynx
the middle part of the throat located behind the mouth
laryngopharynx
the lower part of the throat that connects the pharynx to the esophagus
cricoid cartilage
the only complete ring of cartilage around the trachea
hyoid bone
horseshoe shaped bone in the front of your neck
supports the tongue and plays a key role in speaking and swallowing
carina
a ridge of cartilage at the bottom of the trachea that separates the opening of the right and left primary bronchi
spirometry: pulmonary function test (PFT)
tests pulmonary volumes and airflow times
measures the volumes of your lungs
airflow times = how fast you can breathe in and out a set volume
measures tidal volume
tidal volume
how much air you can breathe in and out of your lungs during each breath
about 500mL going in and out
arterial blood gas
checks oxygen, CO2, bicarbonate buffer, and serum pH
increased CO2 in the blood makes the pH decrease -> more acidic
oximeters
measurement of hemoglobin O2 saturation
pulse oximeter
exercise tolerance testing
aka the stress test
can be used on pts with chronic pulmonary disease
pts walk of the treadmill
want to get to 80% Mac HR
calculated by 220-age = max HR
pt hooked up to an EKG and check BP
complete imaging of the heart and lungs at rest and after the stress test -> ultrasound, chest x-ray
radiography
helpful in evaluating tumours and infections
chest x-ray
bronchoscopy
perform biopsies of the lungs or
check site of lesion or bleeding
uses a bronchoscope with a camera on the end and enters through the mouth
C+S tests for respiratory diagnostic test
sputum testing for presence of pathogens
determine antimicrobial sensitivity of pathogen -> whether is is viral, bacteria, or fungal
general manifestations of respiratory disease
- sneezing
- coughing
- sputum
- change in breathing patterns and characteristics
- dyspnea (SOB)
- cyanosis
- pleural pain
- friction rub
- clubbed fingers/toes
sneezing
(neural reflex from the medulla oblongata):
- reflex response to irritation in upper respiratory tract
- removes irritants from nasal passages
- is associated with inflammation or foreign material
coughing
neural reflex from the medulla oblongata)
- due to inhaled irritants in the oropharynx
- inflammation or foreign material in lower respiratory tract
- dry, unproductive cough = fatiguing
- wet, productive cough = beneficial
- expectorant med or humidifier also helps remove secretions if thick/sticky -> creates more secretions and waters them down
sputum
yellowish-green/cloudy/thick
- often an indication of bacterial infection
rusty or dark coloured
- usually sign of pneumococcal pneumonia
- bit of blood in sputum, some capillary damage in the lungs from infection
large amount of purulent sputum with foul odour
- associated with bacterial infections
- frequent infection may cause bronchiectasis
thick mucus
- asthma or cystic fibrosis
- blood tinged sputum may result from chronic cough -> ruptures capillaries
- may also be a sign of tumour or TB
hemoptysis
- bright red frothy sputum
- associated with pulmonary edema
- fluid in the alveoli getting coughed up
pneumonia
an umbrella term for any infection in the lung
bronchiectasis
scarring, widening of the bronchioles
makes it easier for the airways to collapse
due to chronic damage
lots of mucus and inflammation, will plug the alveoli
less air gets into the lungs
eupnea
normal breathing rate
10-18 breaths per min
kussmaul respiration
“air hunger”
deep rapid respiration -> typical for acidosis, or following strenuous exercise
ok during exercise, bad if at rest
medulla oblongata
breathing centre in the brain
increase in CO2 signals the medulla oblongata to stimulate the diaphragm to breath faster and deeper to get rid of the CO2
laboured breathing
prolonged inspiration or expiration
often associated with obstruction in the airways
wheezing
whistling sounds
indicate obstruction in the small airways
stridor
high-pitched crowing noise
indicated an upper airway obstruction
apnea
cessation of breathing
hyperpnea
increased depth of respiration with normal to increased rate and regular rhythm
faster than eupnea
hyperventilating
cheyne-stokes respiration
periodic breathing with periods of apnea
alternates regularly with a series of respiratory cycles -> gradually increases, then decreases in rate and depth
no breathing .. fast/shallow… bit slower/deeper… fast/shallow… no breathing
ataxic breathing
periods of apnea alternating irregularly with a series of shallow breath of equal depth
apneusis
long gasping inspiratory phase followed by a short, inadequate expiratory phase
rales
light bubbly or crackling sounds with serous secretions in the alveoli
sign of damage or infection
rhonchi
deeper or harsher sounds from thicker mucous
atelectasis
collapsed lung or portion of the lung
dyspnea
feeling short of breath
may be due to increased CO2 or hypoxemia
exercise
if severe it is indicative of respiratory distress
- flaring nostrils
-use of accessory respiratory muscles
- retraction of muscles between or above ribs
orthopnea
occurs when you are lying down
secretions may pool in the lungs, making it more difficult to breath
due to pulmonary congestion
sit pt up
paroxysmal nocturnal dyspnea
- sudden acute type of dyspnea
- common in pts with left side congestive failure
- requires supplemental O2
- occurs typically at night
- sections pool but won’t drain fast enough
pleural pain
results from inflammation of infection of parietal pleura
membrane that sounds the lung
increased pain during inspiration or coughing
rubbing between the visceral and parietal pleura
friction rub
soft sound produced as rough inflamed scarred pleural rub and move against each other
usually paired up with pleural effusion -> build up of fluid between the pleural layers
clubbed fingers and toes
result from chronic hypoxia associated with respiratory and cardiovascular disease
painless, firm, fibrotic enlargement at the end of toes and fingers
looks like grapes at the end of toes and fingers
hypercapnia
increased CO2 in blood
changes in ABGs
could be due to deficit in
RBC
anemia
inadequate perfusion
hemoglobin
CO poison
inadequate cardiac output
blood flow
aging on the respiratory system
- elastic tissues deteriorate, decrease lung elasticity and lowers vital capacity (air that can get into and out of the lungs)
- arthritic changes -> restricted chest movements, reduced respiratory minute volume (how much air can get into and out of the lungs in one minute)
- emphysema (destruction of alveoli and bronchioles) –> can affect individuals over 50, depends on exposure to respiratory irritants, and loss of alveolar septa which is the gas exchange surface area
basic therapies for respiratory disorders
- don’t expose yourself to inhaled irritants -> cigarette smoke
- ensure good ventilation
- up to date on vaccinations, prevent infections and reduce injury to respiratory system
- humidify air -> break down mucus
- moderate exercise
- deep breathing and coughing/ chest physiotherapy
- supplemental oxygen
drugs therapies for respiratory disorders
- decongestants -> vasoconstriction of nasal mucosa
- expectorants -> thins respiratory secretions for easier removal
- antitussives -> reduces cough reflex
- antihistamines -> block histamine receptors to reduce allergic response
- analgesics
- antimicrobials
- bronchodilators -> stimulate beta-2 receptors
- glucocorticoids -> anti-inflammatory
surgical interventions for respiratory disorders
- thoracentesis -> removal of excess fluid from pleural cavity, prevent atelectasis (collapsed lung)
- tracheotomy - incision into the trachea below the larynx
- surgery -> remove lung tumor, abscess, or damaged tissue
pericardium
not expandable
steps to ARDS
- direct lung cell damage and indirect causes (septic shock)
- results in excessive release of chemical mediators
-> increases permeability or alveolar capillary membranes
-> increases fluid and protein in interstitial areas and alveoli
-> fibrous membranes form from protein rich fluid in the alveoli and platelet aggregation , blocks gas diffusion, causes stiffness and decreased compliance
->micro thrombi (mini clots) develop in the pulmonary circulation
-> damage surfactant producing cells
may end of with necrosis and fibrosis -> stiff lung, less compliant, and makes it hard to breathe
ARDS death rate
90% untreated
50% treated
effect of the inflammatory response in the lungs
neutrophils will begin to produce toxic products within the alveoli such as:
- leukotrienes
- oxidants
- platelet activating factors (PAF)
- proteases -> will degrade the protein and lead to the formation of a hyaline membrane creates an added membrane to gas exchange
S+S of ARDS
- rapid onset
- severe dyspnea, rales, productive cough, cyanosis, hypoxemia
- rapid, shallow, respirations -> decreased tidal volume and vital capacity
- increased HR
- restlessness, anxiety -> leads to lethargy, confusion, altered LOC
- combo of respiratory and metabolic acidosis
tx of ARDS
- tx underlying cause
- supply supplemental oxygen
- if person survives, their may be an accumulation of fluid and it could develop into pneumonia -> treat it!
blood gas level in respiratory failure
PaO2 <50mmHg
PaCO2 >50mmHg
will lead to respiratory arrest then cardiac arrest
shock
not enough blood flow to tissues
infant respiratory distress syndrome IRDS
common in premature babies -> 7 to 8 months
inadequate surfactant production -> leads to atelectasis
will follow same steps as ARDS
obstructive lung diseases
- cystic fibrosis
- lung cancer
- aspiration
- obstructive sleep apnea
- COPD -> emphysema, chronic bronchitis, chronic asthma
cystic fibrosis
inherited genetic disorder
autosomal recessive -> have to inherit the mutated allele from both parents
- the CFTR gene, located on chromosome 7, controls chloride ion transport
if there’s a problem in the bodies salt channels, the mucus is not as watery -> thicker and sticky
tenacious mucus from the exocrine glands
primary effacers in lungs and pancreas
cystic fibrosis effect on lungs
- mucus obstructs airflow in bronchioles and small bronchi
- cause permanent damage to bronchial walls
- bacterial infections are common in stagnant mucus -> can cause repetitive pneumonia
cystic fibrosis on the digestive tract
- meconium ileus in newborns (may be the first sign that a baby has CF) -> blocked excretion of meconium (newborns first stool)
- blockage of pancreatic ducts -> blocks digestive enzyme secretion , enzymes start breaking down the pancreas -> may cause type 1 diabetes
- obstruction of bile- ducts c-> blocks fat digestion and fat soluble vitamin absorption (DEAK) -> back uo can cause liver damage
- salivary glands may be mildly affected
- reproductive tract:
- obstruction of the vas deferens
- obstruction of the cervix
- both can lead to sterility
- sweat glands (another first sign that a maybe might have CF) -> sweat with high sodium chloride content, excessive loss of electrolytes during exercise
S+S of cystic fibrosis
- meconium ileus (newborns first stool that is abnormally thick and sticky, blocks the small intestine) -> may occur at birth
- salty skin -> may lead to a sweat test
- signs of malabsorption -> steatorrhea (fatty stool), abdominal distention, constipation
- chronic cough and frequent respiratory infections
- failure to meet growth milestones
- can lead to car pulmonale -> due to pulmonary fibrosis and vasoconstriction, heart has to work harder to push blood into the lungs
diagnosis of cystic fibrosis
- gentic testion
- sweat testing
- stool test
- radiographs
- pulmonary function tests
- ABGs
tx of cystic fibrosis
- chest physiotherapy
- well balanced diet
- regular, moderate, aerobic exercise
average lifespan = 37 yrs
-> due to respiratory failure or cor pulmonale
lung cancer
90% of cases is related to smoking
women are more susceptible
cigarette smoke predisposes to malignant neoplasm because smoking causes metaplasia and dysplasia in the epithelium
detected late usually
early sings:
- productive cough
- facial or arm edema
- headahce
- dysphagia
effects:
- obstruction of airflow
- inflammation and bleeding
- tumor may cause pleural membrane erosion
- paraneoplastic syndrome -> when tumour cells secrete hormones or hormone like substances
systemic signs of lung cancer
- weight loss
- anemia
- fatigue
signs of paraneoplasric syndrome
- indicated by signs of an endocrine disorder
- related to the specific hormone secreted
diagnosis of lung cancer
- imaging -> xray, CT scans, MRI, PET
- chest radiographs
- bronchoscopy
- biopsy
tx of lung cancer
- surgical resection
- radiation
- chemo
- photodynamic therapy (laser to destroy cells)
asthma
chronic inflammatory disease
bronchial obstruction -> severe but reversible periods
in people with hypersensitive or hyper responsive airways
frequent attacks can cause permanent lung damage
may occur as a child or adult
extrinsic asthma
typical onset in children
acute episode triggered by type 1 hypersensitivity reactions (type 1 gives rise to allergies)
- stimuli include an inhaled antigen
-Ige antibodies stick onto mast cells and basophils
- allergic reaction cause bronchoconstriction and mucus secretion
allergic reaction is presented as asthma
intrinsic asthma
onset occurs in adulthood
hyper responsive tissue in airway initiates acute attack
stimuli include
- respiratory infection
- stress
- cold
- inhalation of irritants
- exercise
- drugs
extrinsic asthma steps and effects
- first 10 to 20 mins
- activated mast cells release histamine -> inflammation of mucosa with edema, brochoconstriction, secretion of mucus, partial or complete obstruction of airflow - 4-8 hours
- leukocytosis (proliferation and migration of basophils, neutrophils, and eosinophils), due to the activated macrophages secreting chemokines which attract more WBC
- eosinophils releases leukotrienes prolonging inflammation, bronchonstriction, and epithelial damage - if attack continues…
- partial obstruction due to air trapping, air trapped in the alveoli
- hyperinflation of the lungs -> less force is available to move air out and forces expiration often collapses the bronchial wall - total obstruction
- mucus plug completely blocks air flow, leads too atelectasis
- hypoxemia triggers vasoconstriction of pulmonary partiers, which increases workload for the right side of the hear leading to right sided HF
- more attacks = more damage = lead to COPD
mechanisms of intrinsic asthma
not sure -> chronic T cell activation to internal antigen?
or ANS imbalance?
both types of asthma can lead to damage to epithelial cells, blood vessel proliferation and permanent remodelling
S+S of asthma
- non productive cough (due to thickened mucus)
- SOB
- tight in chest
- wheezing
- tachpnea
- hypoxia
- laboured breathing
- tachycardia
-pulsus paradoxus ( BP differs on inspiration and expiration, large decrease in systolic BP during inspiration >10mmHg)
people can outgrow asthma
risk factors of asthma
- family history -> allergies, possibly genetic
- viral upper respiratory tract infections
- sedentary, obesity, pollutants
- rural kids are less at risk
ABGs in asthma attacks
- respiratory alkalosis
- initially due to hyperventilation - respiratory acidosis
- due to air trapping, less oxygenated blood and CO2 builds up - severe respiratory distress (decreased respiratory effort with weak cough)
- hypoventilation leads to hypoxemia and respiratory acidosis, and loss of cell function - respiratory failure
- PaO2 < 50mmHg
- indicated by decreasing responsiveness, cyanosis
status asthmaticus
- persistent severe attack of asthma
- doesn’t respond to inhalers
- medical emergency
- may be fatal due to severe hypoxia and acidosis -> lead to cardiac arrhythmia/CNS depression
to prevent:
- use peak flow meter
- take meds as prescribed
diagnosis of asthma
- spirometry lung tests -> reduced forced expiratory volume
general
- skin test for allergic reactions
- avoidance of triggers
- good ventilation
glucocorticoids in asthma
blocks chemotaxis of neutrophils and eosinophils
prevention and treatment for chronic asthma
must take before an attack occurs
- leukotriene receptor antagonists
- cromolyn sodium -> reduce WBC activity
- smooth muscle relaxants
cor pulmonale
right sided CHF due to pulmonary hypertension caused by lung damage
emphysema
destruction of alveolar walls
leads to large, permanently inflated alveolar air spaces
progressive difficulty with expiration
increased air trapping, overinflation of lungs, barrel chest
classified on specific location:
centriacinar = enlarged spaces in the central region of the alveoli
panacinar(global) = all of the alveoli sac is affect
contributing factors to emphysema
- genetic deficiency - only 1%, the rest is due to smoking
-> lack of alpha 1- anti trypsin, is needed to decrease elastase activity -> degrades elastic fibres in alveoli - cigarette smoke
- increases number of neutrophils which release proteases -> also decreases alpha 1 - anti trypsin -> more elastase -> more elastic fibre breakdown
- pathogenic bacteria
-> also relates proteases
elastase
released from neutrophils and macrophages as they protect the lungs
breaks down elastic fibres that hold the alveoli open -> increased air trapping
from cigarette smoke or infections
ventilation-perfusion ratio
if there’s little oxygenated blood in the alveoli, the pulmonary arteriole constricts -> in COPD this can lead to pulmonary HTN
if there’s oxygenated blood in the alveoli, the pulmonary arteriole dilates
S+S of emphysema
- slow onset
- dyspnea (difficulty breathing)
- hyperventilation
- barrel chest
- sitting foward
- weight loss
- clubbed finger
tx of emphysema
- avoidance
- immunization
- pulmonary rehab
- bronchodilators
- breathing techniques
- surgical interventions
chronic bronchitis
inflammation, obstruction, from repeated infections
chronic productive cough lasting for 3 months or longer per year in 2 subsequent years
hx of smoking or living in urban area can cause inflammation
leads to hypertrophy or hyperplasia of mucus glands, increased number of goblet cells
can cause pulmonary HTN
pink puffer
= emphysema
blue bloaters
= chronic bronchitis
- cyanosis
- SOB
- excess body fluid, ascites or edema
S+S of chronic bronchitis
- constant productive cough
- tachypnea, SOB
- frequent thick and purulent secretion
- bronchiectasis -> abnormal large bronchioles
polycythemia
abnormally high level of RBC
when someone is hypoxemic, the kidney make more erythropoietin and increases the number of RBCs
tx of chronic bronchitis
- cessation of smoking
- tx of infection
- vaccination
- expectorants
- bronchodilators
- chest therapy
- supplemental O2
- nutritional supplements
pulmonary embolus
- clot or mass that obstructs pulmonary artery or branch
- depends on material, size, location
small emboli may occlude a small area of lung, still be able to live
large emboli may cause sudden death
90% of pulmonary emboli come from DVT
S+S of pulmonary emboli
small emboli:
- transient chest pain, cough, dyspnea
large emboli:
- increased chest pain. with coughing or deep breathing, tachypnea, dyspnea develop suddenly
- vasoconstriction reflex, less blood return to heart, decreased cardiac output
- cough with hemoptysis (blood)
- fever
- hypoxia
massive emboli:
- severe crushing chest pain
- low BP
- rapid weak pulse
- loss of consciousness
risk factors of PE
- immobility -> DVT
- trauma
- surgery to legs
- CHF
- cancer
- long airline flights
- dehydration
atelectasis
non aeration or collapse of a lung
alveoli become airless
process interferes with blood flow through the lungs
gas exchange is impaired
obstructive atelectasis
total obstruction of airway
blocking bronchioles
collapse of alveoli
compression atelectasis
mass/tumor puts pressure on a part of lung causing pressure within the pleural cavity
increased air/fluid/mass leads to loss of adhesions between pleural membranes
pleural effusion
presence of excessive fluid in the pleural cavity
effect depends on the amount of fluid
prevents the expansion of the lung
contraction atelectasis
fibrotic tissue in lungs or pleural
contracts, restricts expansion, leads to collapse
postoperative atelectasis
24-72 hours post surgery
due to pain or abdominal distention (shallow breaths), anesthetics, increased secretions
encourage mobility and deep breathing
transudate effusions
watery effusions due to hypertension
due to HTN
exudative effusion
response to inflammation
protein and WBC leak into pleural cavity
hemothorax
blood in the pleural cavity
empyema
purulent fluid in pleural cavity
pneumothorax
air in the pleural cavity
closed pneumothorax
rib cage intact
simple/spontaneous pneumothorax:
- tear on lung surface
Secondary pneumothorax:
- leakage coming from alveoli -> emphysema bleb
- from a associated respiratory disease
open pneumothorax
puncture wound
sucking wound
large opening in chest wall
may be some movement of the trachea and mediastinum
tension pneumothorax
flap closing over the hole, creates more pressure
will effect the healthy lung as well
traps air in lungs
hypothalamus
produces ADH and oxytocin directly
anterior pituitary gland
produces:
ACTH
TSH
GH
PRL
FSH
LH
MSH
posterior pituitary lobe
releases oxytocin and ADH
lubb
closing of the AV valves
turbulence of the blood that makes the sound
dubb
closure of the semilunar valves
turbulence of the blood that makes the sound
pulse deficit
difference in rate between the apical and radial pulse
the pulse is not reaching the periphery due to decreased stroke volume -> resulting from poor filling or poor ejection
conduction of the heart
- SA node (contracts the atria) -> pacemaker of the heart, will use the cardiomyocytes to conduct to the AV node
- AV node (contracts the ventricles) -> located in the floor of the right atrium
- can become the pacemaker if the SA node stops working - AV bundle (bundle of His)
- purkinje fibres -> terminal fibres
p wave
depolarization of atria
QRS
depolarization of ventricles
T wave
repolarization of ventricles
cardiac control centre
medulla oblongata
controls rate and force of contraction in response to baroreceptors and chemoreceptors
creates either a SNS or PNS stimulation
SNS = increased HR (speed up the depolarization rate on the SA node) -> will dump epinephrine on the SA node (beta 1 receptors)
PNS = decreased HR -> dumps Ach on the SA node -> will depolarize slower by opening K+ channels = hyper polarize
baroreceptors
one in the aortic arch and the carotid artery
detects changes in BP
chemoreceptors
detect changes in blood pH, pCO2, pO2
located in the brain ventricles, aorta, and carotid arteries
cardiac output
CO or Q
blood ejected by a ventricle in one min
CO = SV x HR
average = 4900-5000 mL
stroke volume
volume of blood pumped out of a ventricle per contraction
preload
amount of blood delivered to the heart by venous return
afterload
force required to eject blood from ventricle, determined by peripheral resistance in arteries
left ventricle -> aorta
starlings law
increasing the amount of fluid going into the heart (ventricle fill volume) results in a corresponding increase in the SV
respiratory pump
during inspiration, pressure in thoracic cavity drops which increases pressure in vein in thorax
sucks blood up like a straw
anastomosis
connected between beaches of two arteries
lots occurs in the apex
collateral circulation
if an artery in the heart is blocked, it will release cytokines that will stimulate near by arteries to grow to provide circulation to that area of the heart
right coronary artery
conduction disturbances
nourishes the SA and AV node
