Pulmonary/Pain Flashcards
Airway disorder that is worse on expiration (more force is needed to expel the air out of the lungs)
obstructive pulmonary disorders
examples of obstructive pulmonary disorders
asthma, chronic bronchitis, emphysema
Clinical Manifestations of \_\_\_\_\_\_\_: Dyspnea Wheezing Work of breathing Ventilation/perfusion mismatch Decreased forced expiratory volume (FEV1)
obstructive pulmonary disorders
most common cause for chronic bronchitis and emphysema; contributes to worsening asthma
Smoking
chronic Inflammatory disorder of airways characterized by bronchial hyperresponsiveness and constriction with intermittent periods of reversible airflow obstruction “attacks” (rarely some degree of obstruction that is always present)
asthma
Asthma is a _____ disorder
familial
multiple allergens and microbes may play a role in ________
asthma
theory of asthma cuase that states low exposure to microbes leads to increased development of asthma and atopic disorders; excessive cleanliness is thought to eliminate the microbial stimulation of the immune system that is needed to prevent atopic asthma
Hygiene Hypothesis
Risk Factors for \_\_\_\_\_\_: Family history Allergen exposure Urban living (cockroach/dirt) Air pollution Cigarette smoke Recurrent URIs – especially RSV Other atopic disorders
Asthma
50% of children with _________ will have reoccurring wheezing & eventually diagnosed with asthma within 6 years following the infection
RSV bronchitis
episodic attacks of bronchospasm, bronchial inflammation, mucosal edema, and increased mucus production
patho of asthma
_______ activates the APCs to present to the CD4 T cells in acute asthmatic response
antigen exposure
Clinical manifestations of \_\_\_\_\_\_\_\_\_: Expiratory wheezing Tightness Dyspnea Prolonged expiration Cough- Sometimes (especially in children), cough is the only sign Increased constriction (wheezing with both inhalation & exhalation) Tachycardia = hypoxemia May become status asthmaticus
Asthma
Diagnosis of ______:
FEV1 before & after a short acting bronchodilator is delivered before and after it is given via inhalation
• Will have improvement in expiratory flow volume after the inhaler is used
Asthma
Hypersecretion of mucous and chronic productive cough for at least 3 months of each year x 2 consecutive years
Chronic Bronchitis
Risk Factors for \_\_\_\_\_\_\_: smoking occupational dust chemicals pollution any factor that affects fetal/infant lung growth genetic susceptibility
Chronic Bronchitis
Airway inflammation with an infiltration of neutrophils, macrophages, and lymphocytes into the bronchial walls lead to bronchial edema, increased goblet cells (mucous cells), thick tenacious mucus, poor ciliary action r/t increased in mucus & increased susceptibility to infection, obstruction d/t mucus plugs
Patho of Chronic Bronchitis
Clinical Manifestation of \_\_\_\_\_\_\_\_\_: decreased exercise tolerance wheezing SOB copious productive cough (especially in the AM) polycythemia decreased FEV1
Chronic Bronchitis
abnormal permanent enlargement of gas exchange airways with destruction of alveolar walls without fibrosis; obstruction occurs d/t loss of alveolar elastic recoil that would push the air out of the alveoli
Emphysema
type of emphysema that is autosomal recessive and inherited deficiency of alpha-1 antitrypsin protein involving A1A inhibiting protolytic breakdown of the alveoli **Pts are usually younger than those with secondary emphysema and tested via cheek swab
Primary Emphysema
type of emphysema that is more prevalent and caused by cigarette smoking usually or air pollution /childhood URIs may contribute
Secondary Emphysema
cigarette smoke inhibits antiproteases & stimulates inflammation which increase the protease (enzymes) that attack alveolar walls and diminish elastic recoil which leads to alveoli growing in size and the septa is lost and air is trapped bc it can no longer be squeezed out
Patho of Emphysema
Type of Emphysema:
• Associated with smoking
• Occurs with chronic bronchitis (co-diagnosis)
• Destruction of bronchioles & alveolar ducts in upper lobes
• Alveolar sac remains intact
Centriacinar (centrilobular) Emphysema
Type of Emphysema that is located adjacent to the pleura and septal lines
Paraseptal Emphysema
cluster of aveoli that look like blackberry clusters
acinus
Type of Emphysema:
• Involved the entire acinus
• Alveoli damage is more randomly distributed
• Involves lower lobes of the lung
Panacinar (panlobular) Emphysema
Alveolar Effects of _______:
Mucus in bronchioles
Enlarged alveoli
Fewer capillaries
Emphysema
90% of these are due to blood clots that arise from the pelvis or lower extremities
Pulmonary Embolism
Three Causative Factors of PE called ______:
Venous stasis (sluggish blood flow)
Hypercoagulability
Damage to endothelial lining of the vein
Virchow’s Triad
causes immune response within blood stream that triggers inflammation and coagulation and displaces blood in vessels and leads to wide spread vasoconstriction, atelectasis, pulmonary edema, pulmonary HTN, shock, sometimes death
Amniotic Fluid PE
Clinical Manifestations of \_\_\_\_\_\_\_: Depends on size of embolism S/S may be nonspecific • Restless • Apprehension • Anxiety • Dyspnea • Tachycardia As it worsens: • Chest Pain on inspiration • Hemoptysis
Pulmonary Embolism
condition secondary to pulmonary artery HTN that will cause signs of R sided heart Failure with right ventricular enlargement caused by pulmonary HTN creating chronic pressure overload in the R ventricle
Cor Pulmonale
Clinical Manifestations of _____:
Heart function appears normal at rest
With Exercise: decreased CO, chest pain
Cor Pulmonale
common bacteria of pneumonia
streptococcus pneumoniae
Risk Factors for \_\_\_\_\_\_: young advanced age immunocompromise underlying lung disorder ETOH smoker
Community Acquired Bacterial Pneumonia
a very small bacteria and is commonly seen in summer and fall in children and young adults especially in schools, college dorms, barracks and other places where young people congregate
Mycoplasma
atyplical pneumonia is most commonly caused by ____
mycoplasma
Causes of ______:
Mycoplasma
Legionnaire’s Disease
Chlamydia
Atypical Pneumonia
Common Causes of ______:
o Influenza
o RSV
Viral Pneumonia
immunocompromised people are likely to have __________ pneumonia caused by Pneumocystis or fungal organisms
opportunistic
this is prevalent among patients with CANCER or HIV or other fungal infections
opportunistic pneumonia
the most common route of infection for pneumonia
aspiration of oropharyngeal secretions
Routes of Infection for ________:
aspiration of oropharyngeal secretions
bloodborne (sepsis)
pneumonia
What causes clinical manifestations of pneumonia? (Dyspnea, V/Q mismatch, hypoxemia)
accumulation of consolidated exudate in alveolar air spaces
________ pneumonia does not produce exudative fluid like bacteral pneumonia
viral
pneumonia caused by ______ causes very little mucous production
mycoplasma
Clinical Manifestations of \_\_\_\_\_\_\_\_: chills fever malaise cough that is productive purulent or blood tinged sputum **Crackles/rales** bronchial breath sounds via auscultation over the effected lung tissue
Bacterial Pneumonia
Clinical Manifestations of \_\_\_\_\_\_\_\_: proceeded by an upper respiratory syndrome cold symptoms (fever, non-productive cough, hoarseness, runny nose) **wheezing/fine rales**
Viral Pneumonia
Clinical Manifestations of \_\_\_\_\_\_\_\_: low grade fever cough headache malaise
Mycoplasma Pneumonia
Diagnosis of _______:
H&P
Chest Xray
CBC
Pneumonia
white shadows/opacities in involved area of the lungs seen on chest xray in BACTERIAL pneumonia
parenchymal infiltrates
_____ tuberculosis cases at a rate of ____ cases per 100,000 persons were reported in US in 2016
9,200; 2.9
Risk Factors for \_\_\_\_\_\_: malnourishment immunosuppression living in overcrowded conditions incarcerated persons immigrants elderly
Tuberculosis
acid-fast aerobic bacillus that usually effects the lungs, but may infect other organs
Mycobacterium tuberculosis
Route of Infection for _______:
person to person via AIRBOURNE DROPLETS
by talking, sneezing, coughing, laughing
Tuberculosis
bacteria will lodge in lungs (usually the upper lobes) & cause a mild pneumonitis
-bacilli will migrate to the lymph nodes where t-lymphocytes contact them and initiate cell-mediated response where neutrophils and macrophages engulf and isolate the bacilli—stopping spread by trapping the bacilli and granulomatous lesions (tubercles or Ghon tubercles)—disease then becomes walled off and dormant with no evidence of disease
Patho of TB
reactivation of ________ may occur when the individual’s immune system is impaired by age, disease, or poor nutrition or even re-exposure to the organism
TB
form of TB in which patients do not feel sick and have no symptoms, not infectious and can’t spread to others
BUT is the TB becomes ACTIVE and multiplies that person will develop pulmonary disease at this stage the individual is sick and could spread bacteria to others
Latent TB
Clinical Manifestations of \_\_\_\_\_\_: bad cough that lasts 3+ weeks pain in chest coughing up blood or sputum weakness fatigue anorexia weight loss chills diurnal fever **NIGHT SWEATS
TB
Diagnosis of ______:
Sputum culture: definitive diagnosis, takes 3 weeks for determination
Chest XR: shows Ghon tubercles or cavitation with infiltrates in apex, infected lymph nodes
Skin Test: Mantoux, MOST RELIABLE but does not differentiate from LATENT OR ACTIVE
Blood tests:
***Interferon-gamma release assays
QuantiFeron-TB GOLD (QFT-GIT)-measures how the immune system reacts to the TB bacteria T-Spot
TB
an acute infection or inflammation of airways or bronchi that commonly follows a viral illness
Acute Bronchitis
Clinical Manifestations of ____:
non-productive cough occuring in paroxysms
***aggravated by cold, dry or dusty air
Acute Bronchitis
________ is caused exactly the same way with the same symptoms as pneumonia except there is no pulmonary consolidation and chest infiltrates on chest XR
Acute Bronchitis
_______ in children is a chronic inflammatory disease with sensitivity to allergens, bronchial hyperreactivity, and reversible airway obstruction
Asthma
______ and ______ factors influence severity & onset of asthma.
Environmental and genetic
_______ is a type 1 hypersensitivity reaction that is mediated by IgE
childhood asthma
sometimes the only symptom seen in asthma is cough in children and this is called _____
cough-variant asthma
Clinical Manifestations of _______:
cough
expiratory wheezing
SOB
childhood asthma
Diagnosis of _______:
pumonary fxn tests- spirometry before and after a short-acting bronchodilator
childhood asthma
viral, lower respiratory tract infection, seen in infants and young toddlers, typically in winter and spring,
bronchiolitis
RSV is typical causative agent of ________ (causing 50% of all cases)
bronchiolitis
Causes of \_\_\_\_\_\_\_: RSV influenza strep pneumococci
bronchiolitis
necrosis and destruction of ciliated epithelium cells produces a cell-mediated hypersensitivity to the viral antigen resulting in Inflammation, edema, & thick mucous plugs in the bronchioles which leads to bronchiole spasms and plugs causing narrowed airways, air trapping, and atelectasis
patho of bronchiolitis
Symptoms of \_\_\_\_\_\_\_: o runny nose (rhinorrhea), o tight cough, o fever, o poor feeding, o lethargy, o bronchospasms, and o wheezing, along with o rales, o bronchi, o dyspnea, and o rapid breathing.
bronchiolitis
About 50% of children with _________ by the age of 1 will develop asthma by the time they are 6 years of age.
bronchiolitis
condition that occurs in children, esp. little boys 6mo-3years of age frequently in fall or early winter caused by viral or bacterial infection most commonly (85%) parainfluenza
Croup
Clinical Manifestations of \_\_\_\_\_\_: subglottic edema seal-like barking cough rhinorrhea sore throat low-grade fever.
Croup
Croup is a ______ condition, meaning it gets better on its own although some cases require hospitalization
self-limiting
inflammation of the tonsils most commonly caused by group A beta hemolytic strep that leads to significant swelling of tonsils and posterior pharynx. In some cases, a tenacious membrane will grow and cover the mucosa over the tonsils and sometimes cause an upper airway obstruction…
Tonsillar Infection
_______ can be a complication of infectious mononucleosis, which is caused by the Epstein-Barr virus…also caused by other viruses
Tonsillar Infection
infection behind the tonsil, typically unilateral, pain is usually worse on that same side most commonly caused by streptococcal pharyngitis
Peritonsillar abscess
Complications of ______:
blockage of airway or aspiration pneumonitis.
Peritonsillar abscess
most common potentially life-threatening upper airway infection in children that causes airway edema & copious purulent secretions that lead to airway obstruction that will worsen with the formation of tracheal super membrane and mucosal sloughing.
Bacterial Tracheitis
Causative Organisms of ________:
o streptococcus pneumonia,
o haemophilus influenzae, and
o Moraxella catarrhalis
Bacterial Tracheitis
onset of _______ may be sudden or it may be preceded by viral URI or croup
Bacterial Tracheitis
Clinical Manifestations of \_\_\_\_\_\_\_\_: o increased breathing, o stridor, o hoarse voice, o fever, o cough, o increase secretions of mouth/nose
Bacterial Tracheitis
Severe life-threatening infection of the epiglottis caused by Haemophilus type B (have decreased in incidence since we have the HIB vaccine) however, this problem can be cause by other bacteria, especially strep
Acute Epiglottitis
Clinical Manifestations of \_\_\_\_\_\_\_: high fever severe sore throat unable to swallow saliva inspiratory stridor severe respiratory distress
Acute Epiglottitis
most common age of SIDS
2-4 months
an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage…it is a protective and complex phenomenon made up of sensory experiences, time, space, intensity, emotion, cognition and motivation
pain
Has to do with the amount of pain is associated with how much tissue damage there is. So checking blood sugar (needle prick) is not as painful as a 3 inch laceration on the arm. Accounts for many types of injuries but does not explain psychologic contribution to pain or chronic pain.
Specificity Theory
This describes the role of impulse intensity and re-patterning of the central nervous system. This is a very limited theory because it does not account for all pain experiences
Patterning Theory
This explains the complexities of pain phenomenon. It proposes that a neuro mechanism in the dorsal horn root of spinal cord acts like a gate that can increase or decrease the perception of pain that comes from the peripheral nerves to the central nervous system. The pain is modulated by this gate. Large myelinated A delta fibers move pain signals very rapidly and the brain perceives these signals as stinging, highly localized pain. Where small unmyelinated C fibers move impulses more slowly. These pain transmissions are poorly localized and are dull and achy in nature. These nerves are within the internal organs. These nociceptive transmissions open the gate. Stimuli from non nociceptive transmissions, such as touch and Larger A beta fibers, close or partially close the gate.
Gate Control Theory (1965)
This expands out of the Gate Control Theory. It says that the brain produces patterns of nerve impulses drawn from various inputs, including genetic, physiologic and cognitive experiences. Pain is described as multidimensional. Whole body, mind, spirit experience that recognizes past experiences, culture factors, emotional state, stress regulation, immune system and the immediate sensory input all effect pain perception. For example, labor pain is less intense in a quiet, warm, safe, controlled environment with someone always in attendance. In addition, prenatal education and a birth plan that includes movement, massage and music can greatly enhance the labor experience. This theory illustrates the placidity (adaptable change in structure and function of the brain). Further it proposes that sensory input to the brain produce patterns of pain, but the stimuli may independently originate in the brain with no external input.
Neuromatrix Theory
These begin in the periphery and travel to the spinal gate in the dorsal horn and then ascend to higher centers in the CNS.
Afferent pathways
necessary system for pain located in the brain stem, mid brain and cerebral cortex
interpretive centers
pain pathways that descend from CNS back to the dorsal horn and modulate pain.
efferent pathways
phase of pain response that begins when tissue is damaged by exposure to chemical, mechanical, or thermal noxious stimuli and is converted to electrophysiological activity leading to stimulation of nociceptors
transduction
phase of pain response that involves conduction of the pain impulses moving via sensory A and C fibers into the dorsal horn of the spinal cord and to the brain stem, thalamus and cortex
o “fast” via A delta fibers-skin, muscles
o “Slow” via C fibers-internal organs
Transmission
“fast” pain sensory fibers of the skin and muscles
A delta
“slow” pain sensory fibers of the internal organs
C fibers
phase of pain response which is the conscious awareness of pain involving the sensory discriminating system, effective motivational system, and cognitive evaluative system. This is the awareness and interpretation of meaning of pain
Perception
phase of pain response that is the physiological process of suppressing pain or facilitating pain in an attempt to decrease perception of pain
Modulation
Primary order of nociception of pain consisting of bare nerve endings in the skin, muscle, joints, arteries, and viscera that respond to chemical, mechanical and thermal stimuli
First-order neurons-nociceptors
interneurons in the dorsal horn of the spinal column made up of projection cells that are excitatory or inhibitory interneurons and function as a pain gate to regulate pain transmission, crossover the cord and ascend
Second-order neurons
Afferent neurons in the spinothalamic tract that carry information to the sensory cortex and reticular and limbic system to process and interpret pain
Third-order Neurons
nociceptor fibers for assigned to a particular area of the body surface
sensory dermatomes
The brain is able to localize pain sensation because nociceptor transmission pathways are in anatomical order in the ________ and _______
spinal cord and somatosensory cortex
pain located in the pattern of a dermatome that occurs with spinal nerve injury or area of infection like herpes
radiculopathy
_______ pain does not follow a dermatomal pattern
peripheral neuropathy
physical process of suppressing or facilitating pain
pathways of modulation
This closes the gate, low threshold, mechanical information such as touch, vibration and pressure. For instance, massage will trigger A-Beta fibers to close the gate to more intense C fiber pain felt during the first stages of labor
Segmental inhibition
cerebral cortex, top down, control pathways
Modulation even occur even in the absence of painful stimuli.
Descending Modulation of Pain
spinal medullary pathways that are activated when peripheral pain stimulation remotes from the pain site. This is counter irritation. For example: Sterile water injections on either side of the sacrum as a counter irritant for the first stages of labor.
Diffuse noxious inhibitory controls
Cognitive expectation, the placebo or the non-placebo effect can cause real measurable, powerful, physiological effects that share pathways with pain modulation systems. These modularly pathways modify, dampen or augment nociceptive transmission depending on all the factors effecting the individual, internally and externally.
Expectancy-related cortical activation
these control the emotional and affective responses to pain
Reticular formation and Limbic System
pain excitatory neurotransmitters of pain modulation
glutamate
aspartate
pain inhibitory neurotransmitters of pain modulation
serotonin GABA glycine endorphins enkephalins dynorphins endomorphins
inflammatory (usually excitatory) neurotransmitters of pain modulation
TNF alpha
prostaglandins
bradykinins
threshold of pain
hyperalgesia
neurotransmitters of pain that will lower the threshold of pain
Inflammatory
As tissue heals, this will diminish or continue on as chronic pain
hyperalgesia
threshold depolarization from direct stimuli, like heat, chemicals or tissue trauma
direct excitation
from inflammatory mediators after tissue injury such as loss of oxygen supply or infection.
indirect excitation
Increase excitability of neurons… when normally non painful stimuli causes pain
Central sensitization
when light touch stimulates nociceptors
allodynia
The point at which a stimulus is perceived as pain **Does NOT significantly vary among people or the same person over time.
pain threshold
Duration of time or intensity of pain that an individual will endure before initiating overt pain response
**Very individualized and varies among people or the same person over time.
pain tolerance
Intense pain at one location may cause an increase in the pain threshold in another location. In an individual with many painful sites, may only report the most painful. After the dominant pain is diminished the individual may identify other painful areas.
Perceptual Dominance
this pain treatment stimulates A-beta fibers thereby preventing pain signals from reaching the brain and closes the gate to the C fiber pain of labor.
It can be set to different frequencies, and some will stimulate A-Delta fibers to stimulate the release of endorphins. A counter irritant effect that is not always well tolerated.
TENS Unit
pain treatment that sets up a very painful impulse across A-Delta fibers, rapid stinging pain to the dorsal root quickly, essentially closing the gate to the slower C fiber transmitted pain of first stage of contraction of labor. This counter irritant distracts the patient from the pain and release endorphins. Can last up to 2 hours in patients.
sterile water injections over the sacrum
these decrease the perception of pain by acting like opioids binding with opioid receptors producing sedation and euphoria
endogenous opiate peptides
These are all _______:
Enkephalins, Endorphins, Dynorphins, Endomorphins.
endogenous opiate peptides
these endogenous opiate peptides reside in the hypothalamus and pituitary and are released during times of stress, pain, emotion, while eating chocolate, when laughing, by massage or acupuncture and are called “stress induced analgesia”
Beta Endorphins
strong mu receptor agonists that provide natural pain relief
endorphins
Pain is always a _______ symptom
subjective
pain from tissue injury and will resolve when healed; <3 months (lecture says can last 3-6 months); poorly localized resulting in fewer nociceptors and may be recurrent; a protective mechanism that alerts the body of immediate danger to the body.
acute pain
Clinical Manifestations of \_\_\_\_\_\_ Pain: tachycardia diaphoretic dilated pupils hypertension elevated blood sugar decreased gastric acid secretion decreased gastric motility
Acute
o Pain felt in an area other than the site of injury… in an area that is removed or distant from it’s point of origin… supplied by the same spinal segment.
o Areas of the body share sensory dermatomes
o Embryonic development
o Patterns are predictive-help in diagnosis.
o Can be acute or chronic
Referred Pain
decreased pain threshold and increased response of nociceptors seen in chronic pain
peripheral sensitization
pain that does not respond to usual therapy, and does not serve as a protective purpose…thought to be caused by dysregulation of nociception and pain regulation process
chronic pain
with ______ pain, there will be no sympathetic signs or symptoms-physiologic adaptation occurs and there will be normal pulse and B/P
chronic
injuries to the muscle, tendons and fascia that have occurred that cause spasms, tenderness, and stiffness
Myofascial pain syndromes
these are changes in the PNS and CNS that contribute to allodynia and hypersensitivity.
Chronic Postoperative pain
this is due to growing cancer within an organ or compression of structures by tumor, radiation or chemotherapy tissue destruction
Cancer Pain
very complex type of pain in which nerves become damaged or dysfunctional…may result from trauma or disease to the PNS or CNS and is most often chronic
neuropathic pain
pain caused by injured nerves becoming hyper excitable.
peripheral neuropathic pain
type of pain caused by a lesion or dysfunction in the brain or spinal cord
central neuropathic pain
Clinical Manifestations of \_\_\_\_\_\_ Pain: burning/shooting/tingling sensation of pins and needles stabbing sensation gnawing being miserable
Neuropathic
nociceptor system is functional by _____ weeks gestation
20-24
Children, ages 5-18, have a _____ pain threshold than adults
lower
Signs of \_\_\_\_\_\_\_ Pain: lowered, drawn together brows bulge between brows vertical furrows tightly closed eyes raised cheeks broadened bulging nose open/squarish mouth
Pediatric
Signs of \_\_\_\_ Pain: increased Pain threshold Peripheral neuropathies Skin thickness changes Cognitive impairment Decreased Pain tolerance-women more than men Alterations in the metabolism of drugs and metabolites Impaired renal and liver function
Adult
poor perfusion of a well-ventilated lung
high V/Q
bullae and blebs are associated with ______
emphysema
sterile water injections during labor uses the _______ Theory of Pain
Gate Control
_____ closes or partially closes the spinal gate to pain preception
massage
large myelinated fibers that transmit touch and vibration sensation
A beta fibers
_____ will result in respiratory alkalosis
hyperpnea
allergic asthma due to response to antigen
extrinsic
non-allergic, adult-onset of asthma
intrinsic
COPD patient is cyanotic, they likely have ____
chronic bronchitis
consolidation area of pneumonia will cause auscultation of ________
expiratory crackles/rales
in chronic bronchitis, what causes the JVD and swollen ankles?
R sided heart failure
smoking contributes to bronchial damage in emphysema by
inflammatory release of proleatic enzymes that damage alveolar lining
emotional responses to pain are mediated through ______ and ______
lymbic system and brainstem
what type of nerve fiber transmits dull or achey sensations?
C fibers
In aging, _______ _____________ decreases, and residual _____________ ____________.
vital capacity
volume increases
What kind of V/Q mismatch occurs in asthma?
shunting
reduced oxygenation of arterial blood (PaO2) caused by respiratory alterations
hypoxemia
ischemia- reduced oxygenation of cells in tissues
hypoxia
hypoventilation will show _______ in blood gas
acidosis (too much CO2)
Inflammation from vocal cords to bronchial lumina
patho of croup
Pulmonary System Changes That Occur with \_\_\_\_\_\_: loss of elastic recoil stiffening of the chest wall changes in gas exchange increases in flow resistance
Aging
With aging, lung _______ _______ decreases, _______ ______ increases while lung _______ remains the same.
vital capacity
residual volume
capacity
Alveolar Changes That Occur with \_\_\_\_\_\_ alveolar size increases alveolar surface area available for gas diffusion diminishes airway support decreases
Aging
Respiratory muscle strength/endurance decreases by ___ % by age ___
20% by age 70
Decrease in vital capacity seen with aging leads to decrease in ______ ________ and decreased _______ - _______ ______
ventilary reserve
ventilation-perfusion ratio
Older adults have a decreased compesatory response to _______ and _______
hypercapnia
hypoxemia
Perception of _____ remains the same and can even be enhanced in older adults
dyspnea
PaO2
partial pressure of oxygen in alveoli
With aging, \_\_\_\_\_ declines due to: loss of alveolar surface area thickening of plural septa loss of lung elasticity increase in ventilation-perfusion mismatch
PaO2
Older adults are at greater risk for respiratory depression caused by _______
medications
mucous secreting single-celled exocrine glands in the epithelial lining of the bronchi
goblet cells
respirations with slightly increased ventilatory rate, very large tidal volume, and no expiratory pause caused by strenuous exercise or repiratory acidosis
Kussmaul respirations
alternating periods of deep and shallow breathing with apnea caused by decreased blood flow to the brain stem
Cheyne-Sokes respirations
increased CO2 concentration in arterial blood caused by hypoventilation of the alveoli
hypercapnia
reduced oxygenation of tissue cells
hypoxia (ischemia)
inadequate gas exchange (hypoxemia) with PaO2 < 50 mmHg or hypercapnia with PaO2 > 50 mmHg and pH < 7.25
acute respiratory failure
