Ventilation & Gas Exchange (Ch. 31)-- Definition First Flashcards
Exam 2
Movement of blood through pulmonary circulation
Perfusion
O2 from air in alveoli diffuses into blood in pulmonary capillaries
CO2 moves from blood in pulmonary capillaries into alveoli
Location– Alveolar-capillary membrane
Gas Exchange
- Traumatic
- Tension
- Spontaneous
Types of Pneumothorax
Newborns
- Lack of surfactant
- Aspiration of amniotic fluids
Primary Atelectasis
Adults
- Airway obstruction
- Lung compression– tumor, exudate, pneumothorax
risk factors– sedation, pain, narcotics, immobility
Acquired Atelectasis
Sudden inflammation that starts at the lungs → Disruption of gas exchange at alveolar-capillary membrane
-
Hypoxemia
- Less severe form
Acute Lung Injury (ALI)
- S/S Primary Chronic Lung Disease– Chronic Bronchitis
- Cyanosis
-
Polycythemia
- ⇡ RBCs
- ⇣ SpO2
- Drowsiness
- Altered Mental Status (AMS)
- ⇡ CO2
- S/S R Sided HF
- Venous congestion
- Peripheral edema
- SOB
- Productive cough
Management– Treatment of lung disease & HF, Low-flow O2 Therapy
Cor Pulmonale Manifestations
Collection of fluid in the pleural cavity
Pleural Effusion
Hypoxemia, ⇡ RR, absent breath sounds, dyspnea, chest asymmetry
Treatment– Fix cause, supplement O2, thoracentesis (large needle aspiration)
Tension– ⇡ HR, ⇣ cardiac output, shock, tracheal deviation (treat w/ chest tube)
Pneumothorax Clinical Manifestations
Limited expiratory airflow →Trapped air → Flattened diaphragm
Low V/Q–
- Bronchial Asthma
- COPD
- Cystic Fibrosis (CF)
Obstructive Airway Disorders
⇡ Pulmonary artery pressure with normal LV pressure
d/t– Genetics, Venous HTN, Hypoxemia, Thrombotic/Embolic Disease, Pulmonary Fibrosis
- SOB
- ⇣ Exercise tolerance
- R HF
-
Peripheral edema
- Legs/ankles
-
Functional limitations
- ⇣ ability to perform ADLs
⇡ Pulmonary artery pressure AND HF or Lung Disease
d/t– COPD, HF, Sleep Apnea, PE, Interstitial Lung Disease
-
Chronic Hypoxemia
- Pulmonary blood vessels constrict
-
Resistance to pulmonary venous drainage
- Diastolic dysfunction of LV
- Mitral/Aortic valve disorders
- Chronic thromboembolism
Pulmonary Hypertension Clinical Manifestations
PaO2 < 60 mmHG d/t problem with O2 uptake
Causes– COPD, severe PNA, Atelectasis, ARDS, Pulmonary edema, V/Q mismatch (d/t shunt, dead air space…)
- Decreased O2 to alveoli (d/t high altitude or hypoventilation)
-
Impaired diffusion of O2 from alveoli to blood (d/t V/Q mismatch or alveolar-capillary impairment)
- Vasodilation (Systemic circulation)
-
Inadequate circulation through pulmonary capillaries (d/t pulmonary embolus or arteriovenous malformation)
- Pulmonary blood vessels constrict
Hypoxemic/Oxygenation Failure
Loss of negative pressure in pleural cavity → Collapsed lung
- Pleural effusion
- Pneumothorax
- Atelectasis
Disorders of Lung Inflation
Chest Injury (penetrating or non-penetrating)
- fractured or dislocated ribs
- CPR
- Central line insertion
- Intubation
- Positive pressure ventilation
Traumatic Pneumothorax
Oxygenated Blood
Pulmonary Veins
Movement of O2 and CO2 across the alveolar-capillary membrane
Diffusion
Clear, thin fluid (hydrothorax), specific gravity <1.020
d/t– CHF, renal failure, nephrosis, liver failure, malignancies (cancer)
Transudate
Infection in pleural cavity d/t exudate
Empyema
High V, Low Q (100:1)
- Dead air space
- Low flow states
- Pulmonary embolism (PE)
High V/Q
Exaggerated Type I IgE-mediated hypersensitivity response to inflammatory mediators
Leads to–
- Bronchoconstriction
- Vascular permeability
- ⇡ Mucus production
-
Prolonged expiration → Air trapping
- Lung hyperinflation
- ⇡ Pulmonary artery pressure
Atopic Asthma Etiology
Reduced oxygenation of cells in tissues
- Does not always indicate reduced oxygenation of arterial blood
Hypoxia
- Cyanosis
- Fluid retention
- R-sided HF (cor pulmonale)
- Productive cough
- ⇣ RR
-
Crackles and wheezes
- d/t mucus in the lungs
Chronic Bronchitis Clinical Manifestations
Abnormal elevation of pressure within pulmonary arterial circulation
-
⇣ Size of lumen in pulmonary arteries
- Vasoconstriction → Hypoxia
- ⇡ Inflow of blood to pulmonary arteries
-
Occlusion of outflow of blood from pulmonary circulation
- ⇡ Pressure in LV
Pulmonary Hypertension
⇣ Lung elasticity & abnormal enlargement of air spaces → Alveolar wall & capillary bed destruction
- ⇡ Serine elastase (Protease) release from neutrophils → Digestion of elastic fibers → ⇣ Alveolar recoil
- Lung hyperinflation → ⇡ Total lung capacity
d/t– Genetics, Smoking, Alpha 1 antitrypsin (AAT) (antiprotease enzyme) deficiency
Emphysema Etiology
Pulmonary insult → Inflammatory response (neutrophils secrete proteases, cytokines, & ROS)
⇡ Permeability of alveolar-capillary membrane → Fluid, plasma, proteins, and blood cells into interstitium & alveoli
Loss of surfactant & damage (Type I & Type II pneumocytes) → ⇣ Pulmonary compliance → Lung collapse
Injury to alveolar epithelium → Disorganized repair → Fibrosis → Lungs stiffen (difficult to inflate, ⇡ WOB)
⇣ Gas exchange at alveolar-capillary membrane → ⇡ Intrapulmonary shunting (find alveolus that has O2) → ⇣ V/Q Ratio
Hypoxemia refractory to supplemental O2 → Alveoli collapse
ALI/ARDS Pathophysiology
⇡ RR, ⇡ HR, dyspnea, cyanosis, hypoxemia, decreased chest expansion, absent breath sounds, intercostal retractions
Prevention– incentive spirometer, frequent position changes, ambulate, hydrate
Treatment– fix cause, supplemental O2
Atelectasis Clinical Manifestations
Sudden inflammation that starts at the lungs → Disruption of gas exchange at alveolar-capillary membrane
- Life-threatening Hypoxemia
- Refractory to supplemental O2 Therapy
- Diffuse crackles
-
Dyspnea
- Severe, sudden onset
- w/i 12-18 hrs. of insult
- Hypoxia
- Cyanosis
-
Tachypnea
- ⇡ RR
- Tachycardia
- Diaphoresis
- Sweating
-
Pulmonary infiltrates
- White on x-ray
-
Systemic response
- Multiple organ failure dysfunction syndrome (MODS)
- Renal, GI, CV, CNS
- Multiple organ failure dysfunction syndrome (MODS)
Acute Respiratory Distress Syndrome (ARDS) Clinical Manifestations
Thick mucus hypersecretion → Mucus plugs → Gas trapped in distal portion of lungs
- Lung hyperinflation
- Chronic, productive cough
-
Smoking
- ⇡ mucus production
- ⇡ size and # of mucus glands
Chronic Bronchitis Etiology
Prevention is key
-
DVT Prevention
-
Hospital
- Sequential Compression Devices (SCDs)
-
Heparin (SC)
- 2X/day
-
Outpatient
- Warfarin (PO)
-
Lovenox (SC)
- Low molecular wt. heparin
-
Hospital
-
Multiple or large pulmonary emboli
- Thrombolytic therapy
- Streptokinase
- Anistreplace
- Recombinant tissue plasminogen activators (tPA)
- “clot buster”
- MI/Stroke
- “clot buster”
- Thrombolytic therapy
Pulmonary Embolism Treatment
Reduced oxygenation of arterial blood
- Always leads to reduced oxygenation of cells in tissues
Hypoxemia