Chapter 30: Ventilation and Gas Exchange Flashcards
Hypoxemia
reduction in arterial blood oxygen levels
PaO2 < 80 mmHg
3 ways body compensates for chronic hypoxemia
1) increasing ventilation
2) pulmonary vasoconstriction (improves V/Q ratio)
3) increased production of RBCs (O2 carrying capacity)
______ is a late sign of hypoxemia and can be central or peripheral
CYANOSIS
Central: oral mucosa and lips
Peripheral: nailbeds, nose, or ears
________ provides a direct measure of O2 content in blood and is the best indicator of lung’s ability to oxygenate blood
ABGs
Pulse oximeter is unable to distinguish between ___________
oxygen-carrying Hgb and carbon-monoxide-carrying Hgb
Hypercapnia
increase in CO2 content of arterial blood
3 causes of hypercapnia
1) hypoventilation
2) increase in metabolic rate (fever, exercise)
3) high-carb diet
Obstructive Lung Disorders
increase in resistance to airflow - harder to get air out (increased compliance)
asthma, emphysema, COPD
Restrictive Lung Disorders
reduced expansion of lung tissue with decreased total lung capacity
harder to get air in (decreased compliance)
sarcoidosis, pulmonary fibrosis
Obstructive lung disorders attempt to maintain minute volume by ________ _______ breathing
slow, deep breathing
Restrictive lung disorders attempt to maintain minute volume by ________ _______ breathing
rapid, shallow breathing
Sarcoidosis
restrictive lung disorder in which granulomas are in found in affected tissue and and organ systems
Most common locations for clinical manifestations in sarcoidosis (4)
lungs
skin
eyes
neurological system
Clinical Manifestations of Sarcoidosis
dry, nonproductive cough and SOB
papules and plaques on skin
uveitis
weakness of CN VII = Bells Palsy
Asthma
hyper-reactive (obstructive) airway disease
chronic inflammatory disease that causes episodes of spastic reactivity in the bronchioles
Asthma is characterized by __________ (3)
reversible airway bronchospasm (early) mucus hypersecretion (late) bronchial edema (late)
Immune Cells Involved in ASTHMA (3)
T-helper cells = Th1 and Th2
IgE
Th1
stimulated by microbes or allergens
assists B-lymphocytes to transform into plasma cells (IgE)
Th2
attract mast cells, eosinophils, and basophils = promote inflammation
IgE in Asthma
Allergen binds to IgE
IgE binds to mast cells and provokes degranulation = chemical mediators
Chemical Mediators Released by Mast Cells in Asthma (4)
1) histamine
2) prostaglandins
3) leukotrienes
4) bradykinin
Histamine
attaches to receptor sites in larger cronhi causing swelling and contraction of the smooth muscles
stimulates the mucous membranes to secrete excessive mucus (further narrows the bronchial lumen)
Air trapping is a result of ________ on exhalation (in asthma)
increased intrathoracic pressure that closes the narrowed bronchial lumen completely
Prostaglandins
derived from arachidonic acid - uses the cyclooxygenase pathway
enhances the action of histamine
Leukotrienes
derived from arachidonic acid - uses the lipoxygenase pathway
attach to the receptor sites in the smaller bronchi and cause swelling
bring WBCs to the inflamed area = WBCs form mucus plugs
Bradykinin
proinflammatory mediator
can cause bronchospasms
First-line treatments for asthma (2)
Bronchodilators: Short-Acting Beta2 Agonists (SABA) = albuterol
Inhaled glucocorticoids
Other Pharmacological Treatments for Asthma
Mast cell stabilizer = cromolyn
Leukotriene inhibitors = montelukast
Antihistamines
Concern for Propanalol and Asthma
Propanalol = nonselective beta blocker = can bind to either beta 1 or beta 2 receptors
It can block albuterol’s action
Chronic Obstructive Pulmonary Disease
airflow limitation that is not fully reversible, caused by exposure of the lungs to noxious particles or gases
includes chronic bronchitis, emphysema, and bronchiectasis
COPD = air can get it but can’t get out
This causes:
1) air trapping in the alveoli
2) Retention of CO2
Chronic Bronchitis + Main Cause
increased mucus secretion by the goblet cells of the bronchial tubes, obstruction of the small airways, and presence of persistent, productive cough (>3 mo for 2+ years)
main cause is smoking
Pathophysiology of Chronic Bronchitis
smoking causes chronic irritation of the mucosal lining
goblet cell hyperplasia = secretes excessive mucus
airways accumulate debris
Hypoxia in COPD stimulates pulmonary artery vasoconstriction. This leads to:
increased resistance in the main pulmonary artery
pulmonary HTN
and eventual R-sided HF (cor pulmonale)
Early Signs of Chronic Bronchitis
productive cough with copious amounts of sputum
DOE, normal to low paO2, increased PaCO2
disease progression can be stopped if pt stops smoking
Later Signs of Chronic Bronchitis
Blue Bloater SOB, decreased PaO2 cyanosis air trapping cor pulmonale (R-sided HF)
Emphysema
hyperinflation and decreased elastic recoil cause air trapping in the alveoli = permanent destruction of the alveoli
Centriacinar Emphysema
most common type
related to smoking
localized only to the respiratory bronchioles
Panacinar Emphysema
genetic form
related to alpha-1 antitrypsin deficiency
integrity of alveoli, alveoli sacs, and alveolar ducts is destroyed
Chronic smoking impairs alveolar function through:
1) triggered inflammatory response
2) neutrophils and macrophages release excess proteolytic enzymes = destroy ECM (elastin ) in the lungs = bulla
3) inability of alveoli to recoil and release CO2 = CO2 retention
Deficiency in Alpha-1 Antitrypsin causes:
1) inability to control the amount of elastase produced
2) more elastase = more elastin broken down = destroy lung matrix = reduces elasticity
Early Signs of Emphysema
Dyspnea that progrressively worsens is the first sign
Normal (or slightly dec) PaO2
Normal PaCO2
Late Signs of Emphysema
Pink Puffer tachypnea pursed-lip breathing tripod posture barrel chest low PaO2 and increased PaCO2
Bronchiectasis
uncommon type of COPD
permanent dilation of the bronchi and bronchioles that occurs due to destruction of muscle and elastic supporting tissue
2 Main Etiologies of Bronchiectasis
Mucus obstruction
Persistent infection
Clinical Manifestation of Bronchiectasis
cough with expectoration of copious amounts of foul-smelling, purulent sputum
hemoptysis
weight loss and anemia
Cystic Fibrosis
autosomal-recessive disorder of electrolytes and water ransport that affects certain epithelial cells
caused by a mutation of the CF gene located on chromosome 7
Mutation to the CF gene on chromosom 7 leads to:
impaired electrolyte (chloride) transportation across mucosal surfaces = production of excessive and thick exocrine secretions = leading to obstruction, inflammation, and infection
Mucus Plugging
the formation of tenacious secretions and a reduced ability to clear the secretions
seen in CF
Mucus plugging is the result of:
airway dehydration and thickened mucus caused by:
1) impaired chloride secretion
2) excessive sodium absorption
3) decreased water content in the airway tissues
Airways and lung tissue in CF are characterized by:
air trapping hyperinflation abscess formation lung tissue consolidation lung tissue fibrosis cyst formation
____ and _____ are the two main organs also affected by cystic fibrosis
Liver and Pancreas
Consequences of Liver and Pancreas involvement in CF
bile duct plugged with mucus = biliary cirrhosis lack of pancreatic enzymes decrease in digestion/absorption weight loss fatty stools (steatorrhea)
Standard Diagnostic Test for CF
Sweat Test
a sodium and chloride content twice as high as normal is consistent with CF
Secondary Atelectasis
incomplete expansion of a lung or portion of the lung
collapse of previously expanded alveoli
perfusion occurs w/o ventilation because the collapsed alveoli do not participate in gas exchange
Types of Secondary Atelectasis
Absorptive
Obstructive
Compressive
All three types can cause deoxygenated blood to reach the systemic circulation = hypoxia
Without adequate oxygen = decrease in production of surfactant
Absorptive Atelectasis
surfactant inactivation = surface tension is reduced
less than normal levels of nitrogen being inhaled (can be associated with surgery with general anesthesia)
______ acts as a stent to keep alveoli open
Nitrogen
Obstructive Atelectasis
mechanical obstruction of the airways
secretions, mucus plugs foreign bodies
Compressive Atelectasis
external forces that compress the pleura or lung tissue
pleural effusion, tumors, pneumothorax, or significant abdominal distention
Pleural Effusion
excessive amount of fluid located in the pleural space between the visceral and parietal layers
Pleural effusion results from increased _____________ and decreased __________
increased hydrostatic pressure in the pleural capillaries
decreased colloidal osmotic pressure in the circulatory system
Types of Fluid that can accumulate to cause pleural effusion
transudative
exudative
empyema
chylothorax
Transudative Fluid (Pl. Eff.)
clear fluid with low protein content
most commonly results from heart failure
Exudative Fluid (Pl. Eff.)
cloudy fluid, high in protein
has inflammatory or malignant cells within it
Empyema Fluid (Pl. Eff.)
purulent fluid - contains proteins, leukocytes, glucose, & cellular debris
commonly results from bacterial PNA or a ruptured lung abscess
Chylothorax Fluid (Pl. Eff.)
effusion of lymph fluid in the pleural cavity
milky fluid due to fat-carrying lipoproteins from the GI tract
Clinical Manifestations of Pleural Effusion
Diminished or absent lung sounds *
Tracheal deviation away from the affected side
Dullness on percussion
Decreased diaphragmatic excursion on the affected side and unequal respiratory expansion
Pneumothorax
defined as the entrance of air into the pleural cavity, restricting lung expansion and resulting in a complete or partial collapse of the affected lung
Spontaneous Pneumothorax
occurs when an air-filled bleb on the lung surface ruptures = atmospheric air entering the pleural cavity
alveolar pressure > atmospheric pressure = air flows continues until there is no longer a pressure gradient
Simple (Primary) Spontaneous Pneumothorax
Affects previously health individuals = tall, thin, Caucasian young males
Smoking
Secondary Spontaneous Pneumothorax
Affects those with preexisting lung diseases that cause air trapping and destruction of lung tissue
Asthma, CF, emphysema, tuberculosis
Traumatic Pneumothorax
due to blunt or penetrating trauma to the chest wall
Open = sucking wound; stabbing, GSW
Closed = falls or CPR that results in broken ribs that penetrate the lung
Hemothorax
presence of blood in the pleural cavity usually the result of trauma
Tension Pneumothorax
Intrapleural pressure > Atmospheric pressure
air is unable to escape
compression of the opposite lung, trachea, aorta, and vena cava
EMERGENCY
Clinical Manifestations of Spontaneous Pneumothorax
ipsilateral CP increase in RR asymmetry of chest hyperresonance during percussion decreased/absent breath sounds on affected side
Clinical Manifestations of Tension Pneumothorax
mediastinal shift towards opposite side (trachea)
SV is impaired and CO is decreased
Pulmonary Emboli (PE)
a blood-borne substance that lodges in a branch of the pulmonary artery (emboli) so that flow becomes obstructed
Types of Pulmonary Emboli (4)
1) Thrombus
2) Air
3) Fat
4) Amniotic Fluid
Respiratory Clinical Manifestations of PE
Tachypnea, dyspnea
Cough, hemoptysis
Wheezing, crackles
Central cyanosis
Cardiovascular Clinical Manifestations of PE
Tachycardia
Pleuritic CP - exacerbated by breathing
Neurological Clinical Manifestations of PE
Anxiety
Confusion
Syncope
Clinical Manifestation of Fat Emboli
Petechiae over chest
Pulmonary Hypertension
elevated pressures in the pulmonary artery (>25 mmHg at rest and > 30 mmHg on exertion)
expected MPAP = 15 mmHg
can result in cor pulmonale (RV failure)
Primary Pulmonary HTN
The smooth muscle in the pulmonary artery wall hypertrophies for no reason
Increases vascular resistance
Left ventricular pressure remains normal
Leads to RV failure = cor pulmonale
