Pulmonary Function Alterations

Alterations in Pulmonary Function

• Hypoventilation includes the delivery of air to the alveoli, which is insufficient to meet the need to provide oxygen and remove carbon dioxide with a decreased rate and depth of respiration.
• Hypoventilation results in increased PaCO2 and hypoxemia due to increased alveolar carbon dioxide that displaces oxygen.
• Hypoventilation can be caused by drugs like morphine or barbiturates, disorders like obesity and myasthenia gravis, obstructive sleep apnea, chest wall damage, or paralysis of respiratory muscles.
• Hyperventilation includes an increase in the amount of air entering the alveoli, leading to hypocapnia.
• Chemoreceptors are stimulated by hypoxic which cause hyperventilation.
• Pain, fever, anxiety, obstructive, restrictive lung diseases, sepsis, and brainstem injury can cause hyperventilation.
• A normal physiological response to high altitude causes hyperventilation, which aims to decrease PaCO2 so oxygen can better bind to hemoglobin.
• Hypoxemia includes a deficient blood oxygen measured by low arterial oxygen and low hemoglobin saturation.
• Hypoxia includes a decrease in tissue oxygenation, blood flow, and abnormally low PaO2; a decrease in blood flow means a decrease in oxygen delivered to tissues.

Types of Hypoxia

• Hypoxic hypoxia occurs when PaO2 is decreased despite normal O2-carrying capacity, it is treated with oxygen therapy.
• High altitude, hypoventilation, and airway obstruction can cause Hypoxic hypoxia.
• Anemia hypoxia results from a decrease in O2-carrying capacity and disorders like low hemoglobin, such as sickle-cell anemia, carbon monoxide poisoning, and other anemias.
• Circulatory hypoxia results from low cardiac output with O2-carrying capacity normal, but blood flow is reduced.
• Shock, cardiac arrest, severe blood loss, and heart failure can cause Circulatory hypoxia.
• Histotoxic hypoxia occurs when interference of a toxic substance inhibits the use of oxygen by tissues.
• Cyanide poisoning blocks cellular respiration in all tissues, respiration switches to anaerobic, and lactic acid builds up.

Ventilation-Perfusion Mismatch and Acute Respiratory Failure

• An adequate volume of air in the alveoli should match adequate pulmonary blood flow.
• Ideal state: 4L/min of alveolar ventilation matched to 5L/min of capillary blood flow in the lungs results in a normal alveolar ventilation-to-perfusion ratio of 0.8.
• VA = alveolar ventilation and Q = perfusion/blood flow.
• Low VA/Q : underventilated, equals 2L/min air matched to 5L/min blood flow
• Low PaO2 results in hypoxemia when airways are obstructed.
• High VA/Q : underperfused, equals 4L/min air matched to 2L/min blood flow.
• Pulmonary embolism can block blood flow and cause High VA/Q.
• Shunt occurs when blood passes from the right to the left side of the heart without passing through ventilated areas of the lung.
• An example of a Shunt includes septal defects.
• A Shunt differs from low VA/Q in that alveoli are collapsed, which is not responsive to oxygen therapy.
• Acute Respiratory Failure (ARF) includes a state of disturbed gas exchange resulting in abnormal arterial blood gas values, a PaO2 value of <60mmHg, and a PaCO2 value of >50mmHg (hypercapnia) with a pH less than 7.3 while breathing room air.
• Categories of ARF:
  • Failure of respiration or oxygenation leading to hypoxemia and normal or low CO2 levels.
  • Failure of ventilation leading to hypercapnia.
  • A combination of respiratory and ventilatory failure.
• Lots of conditions can lead to respiratory failure, such as disorders of the neuromuscular chest apparatus (quadriplegia or poliomyelitis), disorders affecting the chest skeletal system (kyphoscoliosis and chest trauma).
• ARF can be caused by shock, pulmonary embolism, or edema, and extreme obesity leading to alveolar hypoventilation.
• Common lung diseases include advanced emphysema, pneumonia, asthma, and acute respiratory distress syndrome (ARDS)
• Manifestations of ARF vary with the cause; general features of hypoxia and hypercapnia that include headache, dyspnea, confusion, decreased consciousness, restlessness, agitation dizziness, and tremors
• Early signs of ARF include rapid, shallow breathing with increased inspiratory muscle activity.
• Late findings of ARF include cyanosis, nasal flaring, sternal/intercostal retractions, cool and clammy skin (due to increased work of breathing), dysrhythmias, and decreased capillary refill.
• Diagnosis is tested by a measurement of arterial blood gases and chest radiography and supporting the test like blood work (high WBCs could mean infection, or low RBCs/hemoglobin indicates anemia).
• Treatment aims to maintain adequate alveolar ventilation through mechanical ventilation, then treat the underlying cause.

Pulmonary Hypertension and Venous Thromboembolism

• Pulmonary Hypertension is a sustained increase in pulmonary arterial pressure above 30mmHg systolic.
• Primary (idiopathic) pulmonary hypertension occurs rapidly, is more common in women, usually present in ages 30s-40s.
• familial, cause unknown but connected to cirrhosis, appetite-suppressant drugs, HIV infection results in a long term poor prognosis
• Secondary pulmonary hypertension results from a known disease process or pathological condition.
• 3 major mechanisms that result in pulmonary hypertension: increased pulmonary blood flow, increased resistance to blood flow, and increased left atrial pressure
• The most common cause of Pulmonary hypertension is increased resistance to blood flow due to hypoxic vasoconstriction (seen in chronic bronchitis and advanced emphysema).
• Other mechanisms that cause increased pulmonary vascular resistance: vasoconstriction due to acidosis, high altitude, obstructive pulmonary embolisms, or damage to capillaries like pulmonary fibrosis or vasculitis.
• Mitral stenosis, and left ventricular failure cause increased left atrial pressure.
• Polycythemia and congenital heart diseases cause increased pulmonary blood flow and viscosity
• Pulmonary hypertension often remains asymptomatic until significant damage to vasculature occurs, and an early sign is often exercise intolerance.
• Patients often experience syncope, increasing dyspnea, chest pain on exertion, fatigue, hemoptysis, and pulmonary edema during pulmonary hypertension.
• Later findings: cor pulmonale and right-sided heart failure due to persistent back pressure to right-sided heart chambers
• Advanced stages: tricuspid and pulmonary valve insufficiency are present
• Chest radiograph showing enlarged pulmonary arteries and right ventricle are often earliest diagnostic tools; ECG can show evidence of right ventricular hypertrophy.
• Treatments aim at reducing vasoconstriction (vasodilators, diuretics, supplemental oxygen, avoiding exercise, and underlying causes; Lung transplants are needed if Pulmonary hypertension is advanced.
• Pulmonary Venous Thromboembolism :Undissolved detached material occludes blood vessels of the pulmonary vasculature, and circulation distal to the obstructed area is impaired.
• Thromboemboli originate in the deep veins of the lower extremities in over 90% of cases.
• Virchow's Triad :
  • Venous stasis/sluggish blood flow, such as bed rest, immobility, congestive heart failure, and obesity.
  • Hypercoagulability, such as oral contraceptives, pregnancy, cancer, smoking, and polycythemia.
  • Damage to the venous wall, such as trauma, penetrating wounds, bone fractures, and burns.
• Thrombi become emboli that travel toward the heart and lung and are most commonly lodged in lower lung lobes due to high blood flow
• If an embolus occludes less than 25% of pulmonary vessels, no changes are seen. If an embolus occludes 25-30% of pulmonary vessels, pulmonary arterial pressures begin to rise and the risk of right-sided heart failure rises.
• Increased pulmonary arterial pressures occur because of vasoconstriction due to mechanical obstruction and the release of serotonin and neural sympathetic stimulation Right-sided heart failure occurs because of high resistance in pulmonary vasculature.
• Cardiac output eventually diminishes enough to cause severe hypotension.
• Acute pulmonary infarction(death of lung tissue due to occlusion) is rare due to alternate circulation options in the lungs, but can occur.
• Presenting symptoms such as initial signs of restlessness, apprehension, and anxiety depend on the size of the embolus.
• The most common symptom is dyspnea, as well as tachycardia and tachypnea.
• Medium to large-sized emboli are associated with sudden dyspnea and severe chest pain, which can progress to heart failure shock and respiratory arrest.
• Diagnosis is completed through helical angiography and pulmonary arteriography.
• If emboli are suspected, prevention is key; treatment includes oxygen support, a constant heparin IV drip, thrombolytic therapy, and filters are also used

Obstructive Pulmonary Disorders and Asthma

• Obstructive lung diseases are manifested by increased resistance to airflow.
• Types of obstructive Lung diseases:
• Obstruction from conditions in the wall of the lumen (asthma, bronchitis).
• Obstruction resulting from increasing pressure around the outside of the airway lumen (emphysema).
• Obstruction of the airway lumen (presence of foreign body, excessive secretions, aspiration of fluids).
• *Major obstructive airway diseases are asthma, bronchitis and emphysema
• Asthma is a lung disease characterized by reversible airway obstruction, airway inflammation, and increased airway responsiveness to stimuli.
• Asthma is characterized by sudden attacks of diffuse wheezing, dyspnea, and cough, resulting from spasmodic contractions of the bronchi.
• Airway inflammation leads to epithelial erosion, mast cell activation, mucosal edema, increased secretions, and smooth muscle contractions.
• Asthma can be classified as non-allergic/intrinsic or allergic/extrinsic.
• Most cases of asthma can be triggered both by allergens and by stimuli such as exercise and exposure to cold air.

Allergic/Extrinsic Asthma and Non-Allergic/Intrinsic Asthma

• 1/3 -1/2 of asthma cases are allergic or Extrinsic asthma, which is associated with a history of hay fever or eczema, positive skin test reactions to allergens, and a family history of asthma.
• The mechanisms stimulating mast cell release are allergic and use Immunoglobulin E-mediated triggers.
• Exposure to a specific antigen that has previously sensitized mast cells in airway mucosa react with antibodies on the surface of mast cells.
• Packets of chemical mediators are released from the mast cells, which are associated with the inflammatory response.
• Asthma mediators cause erosion of the respiratory endothelium and replacement by goblet cells resulting in mucosal edema, inflammatory exudates, and hyperresponsiveness of the airway (bronchoconstriction and leakage).
• Histologic changes in asthma occur in the epithelial basement membrane over time and thickens in asthmatics (17.5µm compared to normal 7µm).
• Parasympathetic stimulation by the vagus nerve'leads to edema, mucus hypersecretion, and bronchoconstriction.
• Non-allergic/Intrinsic Asthma pathophysiology is the same as extrinsic asthma with inflammation of the airways but triggered by antigen-antibody reactions.
• Intrinsic asthma develops in middle age and has less favorable prognosis; attacks are often severe and more difficult to treat
• Airways are very hyperreactive and patients often present with extreme dyspnea, orthopnea, and agitation.
• Some triggers are exercise, occupational substances, drugs, and food additives.
• Exercise-induced asthma includes bronchospasm within 3 mins after the end of exercise and usually resolves in 60 mins; likely the heat and water loss with increased osmolarity of the lower respiratory mucosa releases chemical mediators from mast cells, causing smooth muscle contraction
• Occupational asthma is hypersensitive to exposure to fumes from plastic, formaldehyde, some metals, and textiles; attacks often occur at work and resolve when at home or on vacation.
• Drug-induced asthma attacks can occur within minutes of ingestion and can be delayed up to 12 hours; drug intolerance causes the release of chemical mediators from mast cells resulting in bronchoconstriction.

Asthma Manifestations and Treatments

• Common symptoms of asthma are wheezing, tightness of chest, dyspnea, cough, and increased sputum production.
• Wheezing is caused by air-forcing through narrowed or tight airways.
• Tachycardia is an early sign of hypoxemia.
• Severe attacks of asthma use laboured accessory respiration muscles, intercostal retraction, severe inspiratory wheezing, orthopnea, agitation, tachypnea, tachycardia, and lead to cyanosis, restlessness, and confusion.
• Diagnosis is based on physical findings, sputum examination, pulmonary function tests, blood gas analysis, and chest radiography.
• Patients should avoid triggers related to asthma and receive treatment for respiratory infections early.
• Routine asthma-related drugs focus on decreasing inflammation and bronchoconstriction by using B2-agonists, corticosteroids, leukotriene modifiers, and mast cell inhibitors.
• Severe asthma attacks require immediate epinephrine, subcutaneous terbutaline, and/or aminophylline (fast bronchodilators).
• Aerosol bronchodilating inhalers are typically used to regulate control asthma

Acute and Chronic Bronchitis

• Acute bronchitis is an acute inflammation of the trachea and bronchi, caused by variety of viruses.
• Viruses that cause acute bronchitis include influenza virus A or B, parainfluenza virus, respiratory syncytial virus, coronavirus, and rhinovirus, as well as non-viral streptococcus pneumonia.
• Acute bronchitis can be the result of heat, smoke inhalation, inhalation of irritant chemicals, and allergic reactions.
• The highest incidence is seen in smokers, young children, the elderly, and in winter.
• Airways become inflamed and narrowed from capillary dilation, swelling from exudation of fluid, infiltration with inflammatory cells, increased mucus production, of ciliary function, and loss of portions of the ciliated epithelium.
• Many viruses and mycoplasmic bacteria inhibit macrophages; placing the patient at risk for further bacterial invasion.
• Microorganisms also make airways hyperirritable, causing episodes of bronchospasm
• The presentation of acute bronchitis is usually mild and self-limiting, which includes cough, low-grade fever, substernal chest discomfort, sore throat, postnasal drip, and fatigue.
• Associated inflammation of the larynx and trachea produces croup
• Since it is predominantly caused by a virus, symptoms typically resolve spontaneously in normally health individuals.
• Antibiotics treat Acute bronchitis, if caused by bacteria.
• Codeine-containing medications help to relieve cough by reducing activity in the area of the brain.
• Treatments include increased fluid intake, avoid smoke, and the use of a vaporizer.
• A high potential for bacterial invasion exists; especially in patients with COPD, leading to a serious infection.
• Chronic bronchitis involves hypersecretion of bronchial mucus and a chronic recurrent productive cough of more than 3 months duration and occurring each year for two or more successive years.

• 90% of chronic bronchitis cases are caused by cigarette smoking and repeated airway infections, genetic predisposition, and inhalation of physical or chemical irritants.
• Note: patients with chronic bronchitis and emphysema constitute most cases of chronic obstructive pulmonary disorder.
• Pathologic changes in the airways cause chronic inflammation and swelling of the bronchial walls, scarring, increased fibrosis of the mucosa (lining of the airways ) membrane, hyperplasia of bronchial mucous glands and goblet cells, hypertrophy of bronchial glands and goblet cells, and increased bronchial wall thickness.
• Increased neutrophil activity causes inflammation, and hypertrophy of mucosal glands and goblet cells leads to increased mucus production; Mucus combines with exudates to form bronchial plugs.
• Chronic bronchitis often leads to colonization of H. influenzae and S pneumonia
• Action of mucocillary clearance is impaired some areas of ciliated columnar epithelium are replaced by squamous cells.
• Frequently inflammatory and fibrotic changes extend into surfactant alveoli and prevents oxygenation and increased work of breathing.
• Patients with advanced chronic bronchitis patients appear blueish (cyanotic) and bloated or edematous d/t right-sided heart failure.
• Pulmonary hypertension exists due to compensatory vasoconstriction of the pulmonary blood vessels from increased hypoxia.
• A typical patient is overweight, age 30s or more with shortness of breath and excessive amounts of sputum, chronic cough, and evidence of excess body fluids and a history of smoking.
• Patients often complain signs of chills, malaise, muscle aches, fatigue, loss of libido, and insomnia.
• Cases confirmed through the chest radiograph show: increased bronchial vascular markings, congested lungs, enlarged cardiac silhouette, and evidence of previous pulmonary infection. Physical findings: may show scattered crackles, wheezing, of accessory muscles to breathe, distention jugular venous. congestion, clubbing fingers, ankle edema.
• Overall treatment goals: block the progression of disease but return patient to optimal respiratory function.
• Drugs: inhaled short-acting B2-agonists, anticholinergic bronchodilators, cough suppressants, antimicrobial agents for infections, inhaled or oral corticosteroids, low-dose oxygen therapy. Stop smoking!Reduce exposure to pulmonary irritants inhaled, yearly influenza vaccine, and pneumococcal vaccine.

Emphysema Etiology, Pathogenesis, and Manifestations

• Emphysema includes a chronic obstructive respiratory condition characterized by abnormal, permanent enlargement of alveoli with destructive changes of the alveolar walls.

• It is associated with chronic bronchitis.
• Etiological factors: smoking, air pollution, certain occupations (mining, welding), and α₁-antitrypsin deficiency
• Emphysema develops slowly, so it is more frequently seen in people over age 50.
 If the patient is young to middle-aged: often results from a hereditary deficiency of ɑ1- antitrypsin. This protein inhibits proteolytic breakdown, which degrades lung tissue.

• Pathologic changes leading to alveolar destruction are associated with the release of proteolytic enzymes from inflammatory cells that are released in response to neutrophil, macrophages.

• Damage to the alveolar walls results from smoking
• Smoking causes: Inflammation in lungs tissue
• Inflammation causes: Release of proteolytic enzymes.
• Smoking can inactivate A₁ antitrypsin from normally protects lung tissues.
• Loss in respiratory gas exchange
• Elastic tissue - smaller bronchioles- airway- resistance-decreases airflow as air sacs are destroyed the bronchiols are destroyed air can no longer exit.
• Air can gets trapped in distal alveoli and distend air sacs that obstructed.

Emphysema Classifications and Diagnosis

• 3 classifications of emphysema include Centriacinar, Panacinar, and Paraseptal.
  • Centriacinar emphysema is associated with both smoking and chronic bronchitis that destroys bronchioles.
  • Panacinar emphysema destroys alveoli.
  • Paraseptal emphysema destroys peripheral lung lobules.
• Emphysema causes a progression in alevolar shortness of breathetionality with exercise  Patients often wait to seek help until it is more severe, causing difficulty with exertion

• Patients with advanced emphysema: thin in middle age, who may have a positive history of increasing shortness and can be very dyspnoeic in breath for the past 3-4 years
Patients become skinny d/t energy expenditure - more calorie expending d/t increased respiratory effort and resultant caloric expenditure.

• Patients often use accessory muscles to breath causing progressive dyspnoea,  Use- purse lip breathing to expire more air before small airways and often use body in abnormal postures as forward often leans towards position to breath due to difficulty
• Cough can be present, clenching of the fingers may be visible (rounded fingertip, nail)
- The patient is at risk for developing a pneumothorax and may present with chest pain
 diagnosis based on findings of pts hx, pe, laboratory dx testing, pulmonary function, radiograph artery blood and cardiac EKG’s.

• Chest radiograph will show hyperinflation,
  -Signs: The presence of blebs and bullae.
• Narrowing of chest cavity with small hearts “vertical ” 

• Signs: Decreased breath sounds, no crackles is, during pro-longed expiration, resonance, breathing barrel, an increase diameter on the patient chest.
• Treatment in lung emphysema is most cases is to prevent further progression and manage sx to keep quality life. This is mostly focused on pt w  Chronic bronchitis  (pg. 548)

Emphysema Treatments and Bronchiectasis

• Treatment is as for the same that for patients that have bronchitis Pg.
• Stop smoking!
• Oxygen therapy improves activity can affect tolerance with their condition which is related to life.
• Weight loss must be controlled through adequate nutrition.
• Note: clubbing of the is d/t long term decreased oxygenation in the body, with fibers in the connective areas between the nail and the distal ends.
• Recombinant (synthetic) alpha-1 antitrypsin * (rAAT) (AATD) genetic disease for lung. Produced from yeast and allowing manufacturing and risk of the diseases.
• Bronchiectasis caused by : Dilation of the bronchi; Can be aquired(rare) or coongential. 50% Is associated with Cystic fibrosis. Children is cause to being a higher population. Small, smooth, elastic bronchi often over inflated. Distorted from inflammation to lungs infections. Saccular often shows the distended forms Cylindrical = fusiform/varicose shows with combo

Pathogenesis and Bronchiectasis Treatments

• Bronchiectasis: recurrent infection and to bronchi - dilation (middle), with constant bronchioles. constant Inflammation causing of the walls (obliteration with the destruction of the center ) H. influenza is shows the most in common form infection. ( cilia (columnar- squamous cell. and pus form.
• Patients shows: lots productive chronic, cough; with the yellow/green (putrid). hemoptysis and fevers, sweats is most skin: pallor. And moist (crackles) show halitosis.
• Complications *Recurrent form of bacterial ( viscous  ) Abscesses (visceral). Diagnosis: - H+ and chest x-rays results. ct scan show for best for the decision.
• Treatment: antibiotics. broncos. Chest - drainage. Inhation Need nutrition. Childhood immunizations led decreased in incidence Pleural Air disorder for the space = PNEUMOTHORAX
• ( pleural . PRIMARY: occurs, more tall (20-40 age), and smokers) without disease, with lung ruptures on ribs cages. Springs as the outwards Secondary: caused : Complications : (asthma/infection/Cf -ruptured. Can by cyst. TENSION:: Results ( from truma ) + Air - ( the cannot the collapse + heart to pressure . DECREASE = heart output OPEN is a : “SUCKING “ wounds : heart (opposite - side. from opposite trachea )
• • Tachycardia and affected side, with: 
- Tension = hypotension. ( SubQ) : shift 
-Treatment:: (Chest Tube - greater leaks .) or sealing  is needed

Flail Chest, Pneumonia Bacteria vs Corona

• FLail= trauma, fractured ( ribs sides) → chest wall. Accidents: ( Flail) decrease causes= respiratory or 
tissue compliance. 
seg
 Movement (inward/ out) 
and work in chest / hyPO/ and cx 
Treatment :: (chest , anesthesia PNEUMONIA ACUTE: Inflammation to the the lung tissue in aspirations. flora/inhatations system circulation Pneumonias: aquired viral Normally:(cilia, sneeze , defence ) aqu   viral Bacterial

COVID: attachment to ACE reduced reduced cells - spread cytokine immuniities diabeties