Class 3 Respiratory Flashcards
Pulmonary vasculature
Goes around the alveoli; PEs get caught in the vasculature, not the alveoli
Neurochemical control of ventilation
-Respiratory center, central & peripheral chemoreceptors
-Mechanics of breathing
-Gas transport
-Control of pulmonary circulation
Neurochemical control of respiration
-Chemoreceptors monitor pH, PaCO2 and PaO2
-Located in medulla of the brain
-Monitor arterial blood by sensing changes in the CSF
-Respond to changes in CO2 which combines with H2O to form carbonic acid; hydrogen ions that are capable of stimulating the central chemoreceptors
Peripheral chemoreceptors
-In the carotid and aortic arch
-Respond to changes in PaO2 - activated when it drops below 60 mmHg
-Take over when central chemoreceptors are reset by chronic hypoventilation
-People with prolonged hypercapnia stop responding to CO2
Causes of hypercapnia
-Depression of the respiratory centre d/t medications
-Disease of the medulla, including CNS infections or trauma
-Spinal cord & thoracic cage abnormalities
-Airway obstruction
-Increased work of breathing
Hypoxemia
-Reduced oxygenation of arterial blood
-Caused by respiratory alterations:
-Issues with alveloar gas exchange (V/Q mismatch)
-Perfusion of pulmonary capillaries
Low V/Q
-Air is getting to the alveoli but it is constricted ie. Asthma
-Respiratory rate increases d/t bronchoconstriction
Shunt V/Q
-No gas exchange; less systemic oxygenated blood
-High respiratory rate d/t absent gas exchange
High V/Q
-Something wrong with the perfusion ie. PE, pulmonary HTN
-High respiratory rate because of reduced perfusion
Hypoxemia vs hypoxia
Hypoxemia is low O2 in the blood, hypoxic is low O2 in the tissue
Pediatric airway differences
-Obligate nasal breathing until 3-6 months
-Barrel chests
-Their neck is a bit extended
Continuation of airway
Large occiput-head flexes forward in infancy
LOC dictates
How much O2 is getting to the brain
In a pneumothorax
The chest wall expansion on the posterior side will be asymmetrical
Pediatric vs adut breathing
-6-8ml/kg/min children
-3-4ml/kg/min adults
-In paediatrics: Apnea, hypoxia, poor response to low O2 or high CO2, belly breathers, weak accessory muscles
Influenza pathophysiology
-Upper respiratory virus spread by poor hand hygiene
-Can lead to pneumonia or death
Manifestations of pneumonia
-Cough, fever, myalgia, headache and sore throat
-Mild symptoms similar to a common cold
-Dyspnea, diffuse crackles
Influenza assessment (neuro)
fever, headache, LOC, alert, orientated, lethargic, dizziness, lightheadedness
Influenza assessment (CV)
Hemodynamic status- pale, pink, gray, cyanotic, tachycardia, pulses, capillary refill
Influenza assessment (resp)
-Crackles, impaired gas exchange, tachypneic, cough
Influenza assessment (MSK)
Arthralgia
Lower respiratory conditions
-Disorders of the chest wall & pleura
-Restrictive lung diseases: Aspiration, atelectasis, pulmonary edema, ARDs
-Obstructive airway disorders
-Respiratory tract infections
-Pulmonary vascular disorders
Viral infections may not indicate a
Elevated WBC count
Cyanosis always means
Gas exchange issues
Pleural effusion pathophysiology
-Collection of fluid in the pleural space
-Sign of a serious disease
Transudative effusion (hydrothorax)
-Accumulation of protein and cell poor fluid and caused by:
-Increased hydrostatic pressure found in CHF *
-Decreased oncotic pressure (from hypoalbuminemia) found in chronic liver or renal disease
-Crackles outside of the lung
Exudative effusion
-Accumulation of fluid and cells from an area of inflammation
-Results in increased capillary permeability
-Occurs secondary to pulmonary malignancies, pulmonary infections, pulmonary embolization and GI disease
Empyema
-Pleural effusion that contains pus
-Caused by conditions such as pneumonia, TB, lung abscess and infection of surgical wounds of the chest
Pleural effusion manifestations
-Trapped lung can occur when the visceral pleura becomes encased; pulmonary restriction
-Progressive dyspnea and decreased movement of the chest wall on the affected side
-Fever, night sweats, cough and weight loss
Pleural effusion or thickening assessment
-Presence of fluid subdues all lung sounds
-Tachypnea, tachycardia, dyspnea, cyanosis, dry cough, abdominal distension
-Trachea shifts away from affected side, chest expansion decreased on the affected side
-Bronchial breath sounds heard over the fluid along with bronchophony, egophony, whispered pectoriloquy
Pneumothorax pathophysiology
-Pneumothorax & hemothorax can occur at the same time
-Presence of air in the pleural space that results in a complete or partial collapse of a lung
-Classified as either closed, open or tension pneumothorax
Primary or spontaneous (closed) pneumothorax
-Spontaneous pneumothorax which is the accumulation of air in the pleural space without an apparent event (no external wound)
-Caused by rupture of small blebs on the visceral pleural space; underweight, male, cigarette smokers between 20-40 yrs old
-Line insertion can cause this
Open pneumothorax
-Air enters the pleural space through an opening in the chest wall
-Penetrating chest wound is referred to as a sucking chest wound
Tension pneumothorax
-Pneumothorax with a rapid accumulation of air in the pleural space causing high intrapleural pressures
-Occurs from either open or closed pneumothorax
-Air can enter but not escape
-May occur if chest tubes are clamped or become blocked with a patient who has a pneumo
-This is a medical emergency
Hemothorax
-Accumulation of blood in the pleural space
-Causes include chest trauma, lung malignancy, complications of anticoagulant therapy, pulmonary embolism and tearing of pleural adhesions
Chylothorax
-Presence of lymphatic fluid (chyle) that moves from lymphatic vessels into pleural space instead of passing from GI tract to thoracic duct
-Causes include trauma, surgical procedures and malignancy
Pneumothorax is..
More serious than pleural effusion
Manifestations of a pneumothorax
-Primary; sudden pleural plain, tachypnea, and dyspnea
-Absent or decreased breath sounds
-Tension pneumo; severe hypoxemia, tracheal deviation, and hypotension
Assessment of a pneumothorax
-Absent breath sounds over the affected area
-If a tension pneumothorax develops, the patient may have severe respiratory distress, tachycardia and hypotension
-Mediastinal displacement occurs with tracheal shift
-Changes in BP, pulse, perfusion
About pneumothorax’s
-Causes partial or complete lung collapse, usually unilateral; unequal chest expansion
-If pneumothorax is large, patients may have tachypnea, cyanosis, apprehension, bulging in interspaces
-Tracheal shift, tachycardia, decreased BP
-Decreased or absent breath sounds
Aspiration
-May be related to aLOC, seizure disorders, CVA and neuromuscular disorders that cause dysphagia
-May cause severe pneumonitis
-Lung becomes still and noncompliant leading to edema and collapse
Atelectasis
-Usually occurs after surgery
-Collapse of lung tissue
-Three types which are: compression atelectasis, absorption atelectasis and surfactant impairment
Atelectasis manifestations
dyspnea, cough, fever and leukocytosis
About atelectasis
-Collapsed shrunken section of alveoli, or an entire lung
-Cough, lag on expansion, increased respiratory & HR
-Assymetrical chest expansion, tracheal shift
-Diminished vesicular sounds, occasional fine crackles if the bronchus is patent
Atelectasis causes
-Airway obstruction, the alveolar air beyond it is gradually absorbed by the pulmonary capillaries, and the alveolar walls cave
-Compression on the lung
-Lack of surfactant
Pulmonary edema cause 1
-Valvular dysfunction, CAD, increased left atrial pressure & capillary hydrostatic pressure
Pulmonary edema cause 2
-Injury to capillary endothelium; increased capillary permeability & disruption of surfactant production; movement of fluid & plasma proteins to the interstitial space and alveoli
Pulmonary edema cause 3
-Lymphatic vessel blockage; inability to remove excess fluid from the interstitial space (fluid accumulates)
Causes of pulmonary edema
-Commonly caused by left-sided heart disease
-Capillary injury that increases capillary permeability
-Lymphatic vessel obstruction
Pulmonary edema manifestations
-Dyspnea, hypoxemia, increased work of breathing
-Fine inspiratory crackles
-V/Q mismatch leads to hypoxemia
-Pink, frothy sputum, hypoxemia worsens, hypoventilation with hypercapnia
Pulmonary edema pathophysiology
-When hydrostatic pressure exceeds oncotic pressure fluid moves out into the interstitial space , when the flow of fluid out of the capillaries exceeds the lymphatic system’s ability to remove it, pulmonary edema develops
Severe pulmonary illness/acute lung illness
-Stemmed from the CDC and FDA reports of severe pulmonary illness and deaths related to the use of vaping
-No specific device or substance has been linked to the illness but it is believed to be as a result of chemical exposure
Bronchiolitis obliterans (popcorn lung)
Inflammatory obstruction of the airways
Pathophysiology of acute lung illness (ABDIL)
-Bronchiolitis obliterans (popcorn lung)
-Acute eosinophilic pneumonia
-Diffuse alveolar damage; hemorrhage in alveolar
-Idiopathic interstitial pneumonia
-Lipoid pneumonia
Lipoid pneumonia
Presence of lipids within alveolar space
Idiopathic interstitial pneumonia
Inflammation and scarring in the alveoli
Acute eosinophilic pneumonia
Inflammatory stimulus that recruits macrophages and neutrophils to lung tissue
Manifestations of acute lung illness
-Cough, fever, malaise, fatigue and weight loss
-SOB & dry cough
-Tachycardia, tachypnea
-Potential to develop ARD
-Vomiting and diarrhea
-Scarring, chronic inflammation, cost to treat, addictions
Acute Lung Injury (ALI)
Less severe form of lung inflammation
Restrictive lung disease: ARDS
-Difficult for the lung to expand
-Characterized by acute lung inflammation and diffuse alveolar-capillary injury
Common causes of ARDS
-Sepsis, inhalation of harmful substances, pneumonia, head chest or other major injury
Pathophysiology of ARDS
-Inflammation injures the alveoli-capillary membrane causing pulmonary edema
-V/Q mismatching (shunting)
-Hypoxemia
-Endothelial damage initiates the complement cascade
Endothelial damage initiates the complement cascade
-Toxic mediators such as tumor necrosis factor and interleukin 1 are released
-Alveoli and respiratory bronchioles fill with fluid or collapse
-Lungs stiffen increasing work of breathing, ventilation of alveoli decrease and hypercapnia causes acute respiratory failure
Manifestation of ARDS
-Dyspnea, tachypnea, hypoxemia (unresponsive to O2)
-Lungs stiffen
-Alkalosis then acidosis
ARDS progression
-Starts with dyspnea & hypoxemia
-Hyperventilation & respiratory alkalosis
-Decreased tissue perfusion, organ dysfunction, & metabolic acidosis
-Increased work of breathing, decreased tidal volume, & hypoventilation
-Respiratory acidosis & worsening hypoxemia
-Hypotension, decreased urine output, death
About ARDS
-An acute pulmonary insult (trauma, gastric acid aspiration, shock, sepsis)
-Damages alveolar capillary membrane, leading to increased permeability of pulmonary capillaries and alveolar epithelium
Subjective + ARDS
Acute onset of dyspnea, apprehension
ARDS inspection
-Restlessness, rapid shallow breathing, thin & frothy sputum, retractions
-Decreased PaO2, blood gasses show respiratory alkalosis, radiographs show diffuse pulmonary infiltrates; a late sign is cyanosis
ARDS palpation, auscultation & adventitious sounds
-Hypotension, tachycardia, crackles, rhonci
Pathophysiology of COVID-19
-COV-2 binds to ACE2 receptor, viral RNA released
-ACE II expressed on type II cells
-RAS plays a significant role in COVID-19 infections
COVID-19 assessment (neuro)
fever, headache, LOC, alert, orientated, lethargic, dizziness, lightheadedness
COVID-19 assessment (resp)
-Crackles, gas exchange, tachypneic, cough, cyanosis, pleuritic chest pain
COVID-19 lab values
-CBC: WBC (neutrophils, bands), platelets, hemoglobin
-Electrolytes: sodium, potassium, and BNP levels, creatinine, BUN, GFR, magnesium
-Clotting Factors: INR, PTT, D-Dimer (specific to clots); MISC: CRP, lactate, ABG
COVID-19 pediatrics
-Multisystem Inflammatory Disease
-Increase in children with symptoms of Kawasaki disease
Manifestations of COVID-19
-Fever, rash
-Abdominal & neck pain
-V/D
-Bloodshot eyes, feeling extra tired
