Altered Ventilation and Diffusion Respiratory Structuress3.amazonaws.com/prealliance_oneclass_sample/7KaWvblL2B.pdf• Lung volume reduction or transplant . Smoking: impairs alveolar

Altered Ventilation and Diffusion

Respiratory Structures

Rate and volume of ventilation is regulated by:

1. Functioning respiratory control center (RCC): responds to chemical messages in the

body. Composed of neurons in the pons/medulla. It sends impulses to diaphragm,

muscles to contract/relax. (Constriction= Para, Dilation = Symp)

2. Lung receptors: Located in the epithelium/smooth muscle airways.

3. Chemoreceptors: detect gas exchange needs based on PaO2, PaCo2, pH levels.

Central chemoreceptors: near RCC, respond to pH changes in the CSF. Detects CO2

levels in the blood. (↑ CO2 = ↑ ventilation to expel CO2)

Peripheral chemorecepotrs: sensitive to O2 levels, located in aorta/carotid arteries.

( ↓ O2 = ↑ ventilation)

Alveolar type 1: provide structure and air

exchange

Alveolar type 2: lubricant that coats the

inner portion of the alveolus, promotes

easy expansion, repels fluid accumulation

** inflation would be impossible w/out it

Ventilation: Process of moving air in/out of lungs

• Involves both acquiring oxygen (inspiration) and removing carbon dioxide (expiration)

from the blood

• Neuronal impulses are directed by lung receptors, which map the current state of

breathing and lung function

• Uses the intercostal muscles, diaphragm, and sternocleidomastoid muscles

Inspiration

• Breathing in to acquire oxygen

• Unidirectional from high pressure to low pressure.

• Chest cavity size changes to alter the pressure gradient

• Neuronal stimulation/movement moves diaphragm down and out (reduces pressure inside

lungs to pull air in)

Expiration

• Removing carbon dioxide out of the body through the lungs

• The diaphragm and external intercostal muscles relax

• Lungs compress and increase the pressure inside the airways

• Chest wall moves in and diaphragm moves upwards.

• Inside pressure is more than atm pressure (so air moves OUT)

Measurement of Ventilation

1. Tidal volume (TV): the amount of air exhaled after passive inspiration (air in and out at

rest) ** 500 mL

2. Vital capacity (VC): max amount of air in/out of lungs with forced inhale/exhale

3. Forced capacity (FVC): amount exhaled during forced exhale

4. Forced expiratory volume in 1 second (FEV1): amount exhaled from lungs in 1 sec

5. Residual volume (RV): volume of air left in lungs after maximal expiration

6. Total lung capacity: total air in lungs when they are maximally expanded (VC+ RV)

Diffusion: Process of moving/exchanging O2/Co2 through membranes

• Oxygen and carbon dioxide are exchanged at alveolar capillary junctions

• Two major process occur:

• Oxygen is trying to get to all the cells

• Carbon dioxide is trying to escape the body through the lungs

• Effectiveness depends on: Pressure (Co2, O2 in blood), Solubility (Co2 more soluble),

and Membranes (thickness/SA)

Partial Pressure

• The collision of oxygen and carbon dioxide creates pressure

• PaO2

• PaCO2

Perfusion: Process of supplying oxygenated blood to lungs and organ systems via blood vessels

Respiration: Process in which cells in the body use O2 to make energy

Oxygen Diffusion and Transport

• Oxyhemoglobin (HbO2): As PaCO2 ↑ oxygen dissociates from the plasma and connects

with hemoglobin molecules on RBC’s. Based on attraction to iron. When it is attached to

hemoglobin, it is not available to the cell.

• Oxygen Saturation (SaO2): Attraction of hemoglobin continutes until the hemoglobin

molecules are completely saturated. It is NOT affected by blood volume.

• Once saturation occurs, oxygen continues to diffuse and dissolve in the plasma, until the

partial pressures in arteries = that in the alveoli

Carbon Dioxide Diffusion and Transport

• Dissolved in the plasma (10%)

• Bound to hemoglobin (20%)

• Diffused into the red blood cell as bicarbonate (70%): converted to either carbonic

acid, bicarbonate ions (which helps regulate pH)

Diffusing Capacity

• The measurement of carbon monoxide, oxygen, or nitric oxide transfer from inspired gas

to pulmonary capillary blood and is reflective of the volume of a gas that diffuses through

the alveolar capillary membrane each minute.

Impaired Ventilation

• A problem of blocking airflow in and out of the lungs

• Two major mechanisms implicated:

• Compression or narrowing of the airways

(↑ airway resistance, leading to difficulties with airway clearance, ie. Edema,

exudates or inflammation)

• Disruption of the neuronal transmissions needed to stimulate the mechanics

of the airways

(ignores messages sent by chemoreceptors/lung receptors, ie. Drug overdose)

Impaired Ventilation-Perfusion Matching

• Two possible scenarios:

• Lung are ventilated, but not perfused

• Lung is perfused, but not ventilated

• Impaired ventilation: inadequate o2 comes from lungs even though the blood flow is

ready and able to carry oz.

• Impaired perfusion: the blood flow to the lungs is restricted in one or more areas.

Oxygen might be coming in, but have no blood flow to carry it to the body.

Altered Ventilation and Perfusion

Impaired Diffusion

• Restricted transfer of oxygen or carbon dioxide across the alveolar capillary junction

• Dependent upon:

• solubility and partial pressure of the gas: partial pressure is increased when

molecules are packed in a space, temp increases, when barometric pressure

increases. Decreased oxygen pp can occur in o2 deprevation, hypothermia. CO2

increases with metabolism increase/ exercise.

• surface area and thickness of the membrane

The Effects of Impaired Ventilation and Diffusion

1. Hypoxemia: is decreased oxygen in the arterial blood leading to a decrease in the PaO2.

(caused by o2 deprivation, hypoventilation)

2. Hypoxia: When cells are deprived of adequate oxygen. (widespread hypoxemia)

3. Hypercapnia: a state of ↑CO2 in the blood (CO2 is more easily diffused, so it only really

happens when there is severe alveolar hypoventilation followed by hypoxia).

General Manifestations of Impaired Ventilation and Diffusion

• Local manifestations: usually due to inflammatory processes

• Cough (common, protective), mucus, hemoptysis

• Dyspnea (feeling of SOB), orthopnea (the physical need to sit in an

upright/standing position)

• Adventitious lung sounds (altered) (ie. Wheezing= constricted airway)

• Use of accessory muscles (retractions= the pulling in of accessory muscles to

promote more effective inspiration)

• Chest pain (can originate in the visceral/pleural/airway/chest wall. Pleural pain

increases with deep inspiration and often described as sharp/stabbing pain)

• Barrel chest: due to chronic dilation and distention of the alveoli (i.e

emphysema)

• Systemic manifestations: due to hypoxemia/ hypercapnia

• Fever, malaise, leukocytosis

• ↑ plasma proteins

• Dusky/cyanotic mucus membrane color

• Changes in arterial blood gases

• Mental status changes

• Finger clubbing (painless enlargement/flattening of tips of fingers/toes, caused

by chronic hypoxia)

Laboratory and Diagnostic Tests

• History and physical examination

• Visualization (bronchoscopy, x-ray, CT, MRI, nuclear medicine, etc.)

• Pulmonary function tests

• Pulse oximetry

• Laboratory studies

Treating Impaired Ventilation and Diffusion

• Remove obstruction and restore physical integrity of airways, lung tissues

• Decrease inflammation and mucus; treat infection

• Supplemental oxygen

• Mechanical ventilation

Pneumonia

Pathophysiology:

• Acute infectious process on ventilation/diffusion (caused by miccrorganism, community

acquired: strep/staph/influenza; nosocomial: pseudo/staph)

• Respiratory droplet spread

• Causes inflammation of the lungs

• Occurs commonly in the bronchioles, interstitial lung tissue and/or the alveoli

• Products of inflammation accumulate and cause consolidation (products of inflammation

accumulate as a solid mass)

• 3 stages: 1. Recent infection shows rapid filling of alveolar capillaries with purulent

fluid, 2. Red hepatization: fills with fibrinous exudates, appear as dry red lung tissue,

3. Gray hepatization: WBC’s pack into alveoli as RBC’s degenerate. Pneumococcal

bacteria release toxins that contribute to cell death (forming yellow exudates which are

absorbed and resolution begins).

Clinical Manifestations: Oxygen diffusion is impaired, hypoxia, metabolic acidosis,

dehydration

• Sudden onset of fever

• Chills

• Cough

• Sputum production

• Fatigue

• Loss of appetite

• Dyspnea (SOB)

• Tachypnea (rapid breathing)

• Tachycardia

• Pleuritic pain

• Crackles in lungs

Diagnostic Criteria:


• Complete blood cell count (↑WBC’s)

• Chest X-ray

• Thoracic CT scan (to see areas of consolidation)

• Examine sputum: pneumococcal= bloody/rust color, pseudomonas = green, anaerobic=

foul smelling

Treatment:

• Restore optimal ventilation and diffusion

• Identify pathogen and target with appropriate pharmacologic treatment (with C&S, and

gram stain)


COPD

• Refers to all chronic obstructive lung problems: Emphysema, Chronic Bronchitis and Asthma

• Usually used to denote E+ CB

• Inflammatory processes in both bronchi/ bronchioles

• Progressive, unremitting diseases

Emphysema

Pathophysiology:

• Irreversible enlargement of the air spaces beyond terminal bronchioles

• destruction of the alveolar walls

• obstruction of airflow

• Chronic smoking most often implicated

• Loss of elastic recoil in alveoli leads to airflow obstruction

• Vascular changes: The inner lining of arteries/arterioles become thicker and fibrotic

Clinical Manifestations:

• Persistent cough

• Dyspnea

• Wheezing

• Barrel chest

• Pursed lip breathing



• Pulmonary function tests (↓ AAT)

• Chest x-ray (signs of hyperinflation)

• Hypoxemia (early)/ Hypercapnia (later stages)

• FEV1 is most common test, 6+ seconds is bad

Treatment:

• Maintain optimal lung function in order to allow the individual to perform the desired

activities of daily life

• Smoking cessation

• Pharmacologic therapy (bronchodilators, steroids)

• Lung volume reduction or transplant

Smoking: impairs alveolar function:

1. Inhalation of smoke triggers an inflammatory response

2. Neutrophils/ macrophages are activated and retain in lung tissue

3. They release proteolytic enzymes (proteinases/elastases), that destroy components

of ECM (i.e. elastin)

4. The elasticity of the lung is significantly reduced leading to inability of the alveoli

to recoil and release CO2 into atm.

** Elasticity is key! If the alveoli wall collapses, air gets trapped (which decreases O2 intake and

CO2 release). Hyperinflation results, which makes them get further stretched and continue to

lose elasticity. CO2 retained and pH is reduced.

Chronic Bronchitis

Pathophysiology:

• Persistent, productive cough lasting three months or greater, for two or more consecutive

years

• Result of changes in bronchi/bronchioles:

1. Chronic inflammation and edema of the airways

2. Hyperplasia of the bronchial mucous glands and smooth muscles

3. Destruction of cilia

4. Squamous cell metaplasia

5. Bronchial wall thickening and development of fibrosis


• Cough

• Purulent sputum

• Dyspnea

• Adventitious lung sounds

• Hypoxemia, hypercapnia and cyanosis (more common than emphysema, b/c excess

mucous/obstructed ventilation)


• History and physical examination (recurrent upper/lower resp infections)

• Arterial blood gases


• Pulse oximetry

• Sputum analysis

Treatment:

• Smoking cessation

• Pulmonary rehabilitation

• Pharmacologic therapy


Asthma

Pathophysiology:

• Intermittent or persistent airway obstruction due to:

1. Bronchial hyperresponsiveness (IgE mediators cause edema, bronchoconstriction,

release histamine, prostaglandins, leukotrienes, forms mucous in airways)

2. Chronic inflammation

3. Bronchoconstriction

4. Excess mucous production


• Wheezing and tachypnea, use of accessory muscles

• Dyspnea and coughing

• Chest tightness

• Excessive sputum production

• Anxiety

• Hyperventilation can lead to respiratory alkalosis



• Evidence of respiratory distress

• Pulsus paradoxus: exaggerated decrease in systolic BP during inspiration

• Wheezing

• Prolong expiratory phase

• Atopic dermatitis: eczema, hypersensitivity reactions on skin.


• Laboratory studies

• Chest x-ray

Treatment:

1. Monitor lung function

2. Control environmental triggers

3. Pharmacologic therapy

4. Patient and family education; action plan

Cystic Fibrosis

Pathophysiology:

• Autosomal recessive disorder of electrolyte and water transport affecting certain

epithelial cells (respiratory, digestive, and reproductive lining)

• Mutation of the CF gene (both parents have to have it); inability of epithelial cells to

conduct Cl; and therefore transport water across mucosal surfaces leads to thick

secretions and obstructions in the resp tract

• Associated with mucus plugging, inflammation, and infection in the lungs; also affects

other body systems

• Respiratory failure is most common cause of death


1. Reproductive: Men get infertile (clogs vas deferens), but the women get altered menses

2. Respiratory: respiratory infections, chronic cough, sputum, vomiting, tachypnea,

wheezing, crackles, chest pain, respiratory distress, cyanosis, barrel chest, recurrent

sinusitis, nasal polyps

3. Gastrointestinal: ↓Cl secretions, get large, greasy BM’s. Get inflammation/scars which

increase bowel obstructions, poor fat absorption, weight loss



• Sweat test (Since there are problems with the Cl channels, get salty deposits on the skin)

• Genetic testing

• Chest x-ray (see how much secretions)

• Sputum analysis

Treatment:

• Respiratory

• Chest physiotherapy (press on back)

• Pharmacologic treatment (aerosol to thin secretions)

• Lung transplant (extensive scarring/cysts on the lungs)

• Gastrointestinal

• Optimal nutrition

• Pancreatic enzymes

Mucous plugging: (result of)

1. Greater mucus production

2. Airway dehydration, due to thickened mucus caused by impaired cl secretion, excess Na absorption, decreased

water

3. Adherence of mucus to epithelium with impaired cilia

Acute Respiratory Distress Syndrome: ARDS

Pathophysiology: Sepsis is most common cause

• Lung injury to respiratory distress within 24-48 hours

• Severe acute inflammation and pulmonary edema without evidence of fluid overload or

impaired cardiac function

• pulm edema, damages alveolar capillary junction, damage to type II cells, increased

protein, disruption of surfactant = atelectasis, alveolar collapse)

• Mortality rate 30%-40% from multi-system organ failure in those untreated


• Tachypnea

• Dyspnea

• Retractions

• Crackles due to fluid accumulation

• Restlessness, anxiety


• History and physical examination (lung injury)

• Arterial blood gases: depict hypoxemia/hypercapnia resp. alkylosis

• Laboratory studies (blood cultures to detect sepsis)

• Imaging studies

Treatment

• Remove causative factors

• Administration of 100% oxygen

• Mechanical ventilation

Documents

Altered Ventilation and Diffusion Respiratory Structuress3.amazonaws.com/prealliance_oneclass_sample/7KaWvblL2B.pdf• Lung volume reduction or transplant . Smoking: impairs alveolar