Ventilation and Gas Exchange Disorders

• The presentation is about disorders of ventilation and gas exchange, covering pathophysiology.

Respiration

• The primary function of the respiratory system is gas exchange between atmospheric air in alveoli and blood in pulmonary circulation.
• Ventilation involves air movement into and out of the lungs.
• Diffusion involves the movement of oxygen and CO₂ across the alveolar-capillary membrane.
• Perfusion involves blood movement through pulmonary circulation. -The alveolar-capillary membrane is where gas exchange occurs.

Physiologic Effects of Ventilation and Diffusion Disorders

• Hypoxemia refers to the reduced oxygenation of arterial blood.
• Hypoxia refers to the reduced oxygenation of cells in tissues.
• Hypoxemia leads to hypoxia, and hypoxia can lead to hypoxemia.
• Pulse oximetry and arterial blood gas (ABG) are measures of blood oxygenation.

Causes of Hypoxemia

• Decreased O₂ delivery to alveoli is caused by reduced O₂ in the air and hypoventilation.
• Impaired diffusion of O₂ from alveoli to blood can occur with V/Q mismatch and alveolar-capillary membrane impairment.
• Inadequate circulation of blood through the pulmonary capillaries can result from arteriovenous malformation and pulmonary embolus.

Ventilation and Perfusion Mismatch

• Gas exchange properties of the lung depend on matching ventilation (V) and perfusion (Q, blood flow).
• The ventilation-perfusion ratio (V/Q) should ideally be 1:1.
• V/Q mismatch is the most common cause of hypoxemia, with a V/Q ratio not equal to 1:1.
• A shunt is perfusion without ventilation -Examples of shunts: atelectasis, pneumonia, obstructive lung diseases, asthma, chronic bronchitis, emphysema, acute respiratory distress syndrome (ARDS). The V/Q ratio in this case is low, such as 1:100.
• Pulmonary embolism is an example of a "dead air space" that describes ventilation without perfusion; the V/Q ratio is high (100:1).
• Both dead air space and shunt cause hypoxemia.

Hypoxemia: Clinical Manifestations

• Hypoxemia affects tissues, activating compensatory mechanisms.
• Brain, lungs, and heart need more oxygen.
• Decreased O2 causes anaerobic metabolism → lactic acid production and metabolic acidosis.
• Acute hypoxemia causes mild SNS activation like increased heart rate, increased respiratory rate, decreased mental acuity, vasoconstriction, pale skin, and diaphoresis.
• Moderate or severe acute hypoxemia causes altered mental status, stupor, or coma.
• Chronic hypoxemia causes increased respiratory rate, pulmonary vasoconstriction, polycythemia, cyanosis, and clubbing.

Hypoventilation

• Hypoventilation is characterized by a low respiratory rate resulting in CO₂ retention.
• Inadequate alveolar ventilation occurs in relation to metabolic demands under hypoventilation.
• CO₂ removal is less than than CO₂ production → hypercapnia/hypercarbia → respiratory acidosis.
• It increases CO₂ concentration in arterial blood.
• Causes may include brain injury, sedation, obstruction of the airway, or physiologic dead space.
• Elevated CO₂ detected by ABG results aids diagnosis.

Hyperventilation

• Alveolar ventilation is greater than metabolic demands.
• CO₂ removal is greater than CO₂ production → hypocapnia/hypocarbia → respiratory alkalosis.
• Anxiety, pain, and hypoxemia can cause hyperventilation

Disorders of Lung Inflation

• Airway air inflates lungs & negative pressure in pleural cavity (intrapleural pressure) prevents lung collapse
• Lung collapse results from disruption of pleural cavity or loss of negative pressure.
• Disruption of pleural cavity leads to pleural effusion, pneumothorax, or atelectasis.

Pleural Effusion

• An abnormal accumulation of fluid in the pleural cavity.
• Transudate, Exudate and Hemothorax are three example manifestations.
• Transudative pleural effusion is a clear fluid caused by increased hydrostatic pressure or low plasma oncotic pressure, such as in congestive heart failure, cirrhosis, nephrotic syndrome, pulmonary embolism, or hypoalbuminemia.
• Exudative pleural effusion is a cloudy fluid caused by inflammation with increased capillary permeability, such as in pneumonia, cancer, TB, viral infection, pulmonary embolism, or autoimmune diseases.
• Hemothorax is blood in the pleural cavity, from chest injury, chest surgery complications, malignancies or an aortic aneurysm rupture.
• Hemothorax treatment: chest tube

Pleural Effusion: Manifestations and Treatment

• Causes: fluid build-up
• Symptoms: lung expansion decreases, dullness to percussion, decreased breath sounds, dyspnea, hypoxemia.
• Treatment: fix the cause, antibiotics, thoracentesis (large needle aspiration), chest tube.

Pneumothorax

• Pneumothorax involves air in the pleural space leading to thoracic structure displacement with partial or complete lung collapse.
• Three types: spontaneous, traumatic, and tension pneumothorax.

Spontaneous Pneumothorax

• The cause is unknown but involves a ruptured air-filled bleb located at the top of the lungs.
• Likely thin, tall people or smokers
• It can occur in persons with lung disease such as asthma, TB, cystic fibrosis, COPD, or lung cancer, and is potentially life-threatening

Traumatic Pneumothorax

• Pneumothorax is a result of penetrating or non-penetrating chest injuries or fractured/dislocated ribs penetrating the pleura.
• CPR, central line insertions, intubation, positive-pressure ventilation are some other causes of pneumothorax

Tension Pneumothorax

• Air enters pleural space and does not exit which causes intrapulear pressure that exceeds atompsheric pressure
• Tension Pneumothorax is life threatening, causes compression atelectasis and can cause the trachea and sternum to shift to the left.
• This causes the mediastinal shift, vena cava compression, ↓ venous return, and↓ cardiac output

Pneumothorax: Clinical Manifestations and Treatment

• Symptoms: Respiratory Rate, dyspnea, chest asymmetry,↓or absent breath sounds, tracheal deviation, ↑HR, ↓CO, hypoxia, and shock
• Treatment: fix cause, supplemental O2, Thoracentesis, and Chest tube insertion

Atelectasis

• Atelectasis is an incomplete expansion of lung tissue of newborns
• Lack of surfactant in premature neonates or aspirated amniotic fluid are conditions that cause Atelectasis in newborns
• Pleural effusion, pneumothorax, or loss of pulmonary surfactant are other causes
• Adults can acquired Atelectasis acquired through an airway obstruction caused by a tumor or exudate for example, also lung depression or sedation
• A patient is at risk of developing Atelectasis if sedated, in pain, on narcotics and immobile.

Atelectasis: Manifestations, Prevention and Treatment

• Symptoms: ↑RR, ↑HR, dyspnea, cyanosis, hypoxemia, ↓chest expansion, decreased or absent breath sounds, inward pull of intercostal muscle
• Prevention: Incentive spirometers, deep breathing, coughing, frequent position changes, ambulation, and hydration
• Treatment: Treat causes or give supplemental O₂

Obstructive Airway Disorders

• Impaired expiratory flow and low V/Q ratio are characterisics of obstructive Airway dirsorders
• This can be caused by, bronchial asthma, COPD or cystic Fibrosis
• Trapped air can occur in some conditions and a flattend diaphram as well

Bronchial Asthma

• The disease is a chronic inflammatory condition that involves recurring airflow obstruction and airway hyperresponsiveness.
• Asthma can be triggered by respiratory tract infections, exercise, drugs (ASA and morphine), emotional upset and bronchial irritants (cigarette smoke).

Bronchial Asthma: Pathophysiology

• Asthma is an exaggerated type I IgE-mediated hypersensitivity response releasing of inflammatory mediators where
• • Bronchoconstriction
• • Vascular permeability
• • ↑ mucus production occurs
• Prolonged attacks trap Narrowed airway leading to hyper-inflamation, air trapping, increase in pulmonary artery pressure and Prolonged expiration

Bronchial Asthma: Early Phase Response

• Early phase responses to to extrinsic allegens occur 5-30 mins post exposure and last around an hour.
• Early phase includes:

Release of inflammatory mediators Vasodilation Damage Bronchospasm

• Treatment includes:

  bronchodilators such as albuterol

Bronchial Asthma: Late Phase Response

• Extrinsic allogen that occurs after 2-8 hours of exposure
• Includes:

Mucosal Edema Increased Section ^WBC Epithelial Damage Bronchospasm

• Lasts days and treat with corticosteroids

Bronchial Asthma: Manifestations

• Airways narrow due to bronchospasm, bronchial mucosal edema, and mucus plugging.
• Expiration is prolonged due to airway obstruction.
• Trapped air behind the occlusion causes hyperinflation of lungs (air trapping).
• An increased work of breathing results in increased O2 demands, dyspnea, and fatigue.
• Decreased Alveolar ventilation causes V/Q mismatch, hypoxemia, and hypercapnia.

Bronchial Asthma: Treatment

• Treatment begins by Avoiding contact with Allergens by the patient
• Immediate treatment involve Pharmacologic therapy, with Albuterol (B2-agonist)
• Bronchodilation, and bronchial smooth muscle relaxation
• Corticosteroids (reduce airway inflammation.)
• Long term is treated with Inhaled corticosteroids (mometasone) and/or inhalation of long-acting ẞ2-agonists (salmeterol)
• Another strategy is combination inhaled medications (Symbicort)

Obstructive Lung Diseases: COPD

• COPD is a combination of lung-related conditions that causes airflow obstruction, such as chronic bronchitis and hyperinflation
• The condition is persistent, most common and progressive.
• COPD Risk factors include:

  Tabacco Smoke Occupaational Dust Air pollution Chemicals

• There are 2 Type

  Chronic Brinchitis emphysema

COPD: Emphysema

• Loss of lung elasticity and abnormal Enlargement of air spaces; alveolar wall and capillary bed destruction,
• Leads to Hyperinflation of lungs and ^ TLC Causes: due to Smoking, Lack of AAT) A(protease enzyme
• Serine Elastance Digests and causes loss of Elastic Recoil in alveoli

COPD: Chronic Bronchitis

• Chronic production and Chronic cough for 3 months of the year and 2 consecutive years ^ Mucus production and mucus Thicker than normal leading to trapping gas in distal portion of lungs resulting in Hyperinflation and chronic product cough

COPD: “Pink Puffers” vs “Blue Bloaters”

• "Blue Bloaters" (Chronic Bronchitis): -Cyanosis, history of smoking, and barrel chest, Fluid retention, Productive cough, Polycythemia, RRhypoventilation, crackles, and wheezes.
• "Pink Puffers Emphysema":
• No cyanosis, history of smoking and or barrel chest, but Prolonged expiration and Increased Accessor muses breathing
• Decreased breathing, Increased RR,Wheezing

COPD: Diagnosis

• To establish a diagnosis do a history and physical exam

  Chest X-ray

Lab work PFT's

COPD Treatment

• The goal of CDOP is to avoid triggers such as bronchospasm, prevent respiratory infections encourage pneumonia vaccine, restore lung function and efficiency and reduce work of breathing of pharmacologic therapy

  bronchodilators anticholinergics Inhaled or PO coricosteroids

Cystic Fibrosis

• An inherited autosomal recessive disorder involving the excocrine glads in epitheal in respiratory GI, and reproductive traccts
• Chronic respiratory diseases results in :

Pancreatic deficiency High ^ Sodium chloride in sweat

• Mutation in cystic fibrosis

  Choldie Channels impaired in airway epithelial cells

Mutations makes it impermeable to chloride

Cystic Fibrosis: Pathogenesis

• A key pathway of Cystic fibrosis is impaired transport of Chloride into alway Lumen making Sodium ^ H29 to move from airway into blood which ^ respiration and makes thick secrition
• Decreased levels of H29 in mucociliary blanket -Dehydration in ^ accumulation due to airway obstructions

Causes risk of pulmonary infection Mucus in Pancreatic and biliary ducts and Vas deferens that resales a Zoosperimia

Cystic Fibrosis: Manifestations

• Accumulation of thickened mucus in bronchi
• Impaired mucociliary clearance
• Lung infections _ Chrinic bronchiolitis and Bronchitis
• Abnormal exocrine pancreatic function (increased mucus production can damage certain organ)
• Steatorrhea, Diarrhea, abdominal Pain Malnutrition
• Diagnosis is based on: Respiratory and GI manifestations
• Positive new born screening due to High immunoreactive trypsinogen
• Lab tests such as:

Sweat Chloride tests (2X ) Functional tetsting

Cystic Fibrosis: Treatment

Goal: slow progression of secondary organ dysfunction

• Cronic lung infections can be treated by bronchodial tors and physiotherapy _ Pancreatic insurfiancy

Pulmonary Embolism PE

• Lodging of substances that blocks blood flow to the pulmonary artery in the lungs causing air space which cause air space -> High Ventilation perfusion :100:1.

PE: Risk Factors

• Risk of infection with pulmonary emboli can increase with triad and endothelial injury or state hypercoagulability

• venous endothelial

• injury ^ prolonged bed rest

• ^pregnancy and cancer

PE Clinical Manifestation

• Pulmonary Embolism can depends on a size and location
• Small Emboli tend to be in the asymptomatic where a Moderate size emboli can cause rapid shallow pleurisy chest pain
• A big emboli causes sudden collapse crushing chest pain

PE: Treatment

Prevention key by DVT Prevention:

• ^Hospital; Sequential compression device. subcutaneous Heprin
• Ambulant: warfarin and level molecular weigin heparin
• Large: thrombolytic therapy streptokinase

Pulmonary Hypertension

• Hypertension occurs when pressures elevate abnormally Within pulmonary arterial
• Can be caused a lumen of arterial ^ Vasoconstruction due to hypoxia ^ occlusion (High Blood Pressure)

Pulmonary Hypertension Manifestations

• Higher pressure, shortness of breath
• Low exercise
• Right sidled heart _ Peripharal Eddmia __Diastonic disfunction of LV in mitral valve disorder

Cor Pulmonale

• Right heart failure resulting from lung disease or pulmonary Hypertensions _ ^ pulmonary circulation
• Sign and symptom of pulmonary lung,
• Cyanosis of the skin and Polycythemia. LOW SPO2 and drowsniess and altered mental
• Sign is righted-side HF
• Venous congestion shortness of breath and a productive cough
• LOW FLOO2 and therapy

Acute Lung Injury/Acute Respiratory Distress Syndrome

• Disrupted gas exchange at the alveolar–capillary membrane resulting in : Life threatening high risk or ^ marbity ^ acute respiratory distress syndrome :
• diffucs and serve dyspnea
• tackicardia

ALI/ARDS: Causes

• Aspiration: of H2O
• Drugs and toxins: Heroin and coicain
• Infection and COVID +Traumna and Chnest Traumna
• Multiple transfusions

ALI/ARDS: Pathophysiology -ARDS

• In both of ALI/ARDS that are a ^ preminability which ^ domage to cell type

• causes Allevi collapse
• low-permeability compramises Allevi
• High WOB due to stiffened Luyng

ALI/ARDS Manifestation

• Rapid onset respiratory distress 12-18 hours +Hight or low RR signal
• Marked hypoxemia to supplemental ^2 therapy
• Organ Falioure system response

ALI/ARDS: Treatment

• Oxegenate longs and Vitals organs Recognizing treat underlying condition _ Prevent further lung injury or treatement and complication

• Low mortality rate

• Trach care

• intubate +Ventialte