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BIO 250 – Patho II- Respiratory- Lewis chapters: 26-28

Chapter 26 – Respiratory System should be a review from A/P – On your own but remember there will be exam questions from this chapter/study guide pages.

Respiratory function: exchange of gases between environment and blood; lungs, chest wall, airways, pulmonary circulation. Braun Fig. 13.1 Ventilation and Diffusion are BOTH required

I. Airway defenses:a. Nose filters the air we breathe, also warms and moisturizes it. The movement of air

through the pharynx allows larger particles to be trapped there.b. Mucociliary clearance: cilia and mucus trap particles and move them up to be coughed

out.c. Cough reflex: clears the debrisd. Reflexive bronchoconstriction: bronchi constrict when irritants are presente. Alveolar Macrophages: reside below the bronchioles and engulf debris and pathogens.

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II. Ventilation: Lungs are ONLY mechanism for these to happena. Inspiration – acquiring oxygen from the environment

i. Process of breathing – air moves from high pressure to lowii. Drop of diaphragm and chest expansion (intercostal muscles move chest out)

decreases pressure inside the lungs so air moves from environment into lungs.b. Expiration – removing CO2 from the blood

i. Diaphragm and intercostals relax = chest wall moves in and increases intrathoracic pressure = air moves out.

What happens if your patient has….ascites (fluid accumulation that interferes with the diaphragm? Or broken ribs…. What happens to their breathing?)

c. Rate and volume controlled by:i. Respiratory center in the brain

1. Increases or decreases rate and depth based on chemical information from the body

2. ANS also innervates lungs causing bronchodilation or constriction of the smooth muscles in the bronchi. Which neurotransmitter causes which?

ii. Lung receptors1. Sensitive to irritants = cough2. Promotes expiration

iii. Chemoreceptors1. Sense PaO2, PaCO2, and pH levels – this information is sent to

respiratory center in the brain.2. Peripheral chemoreceptors located in aorta and carotid arteries sense

the level of PaO2 – increase ventilation when this drops.

How does the respiratory center respond to acidosis? Alkalosis? What impact does anesthesia have?

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d. Work of breathing is easier with:i. Good lung compliance (allows max inspiration)

1. Ability of the lung tissue and chest wall to expand a. Surfactant – lipoprotein that promotes expansion and repels

fluid accumulation. The presence of this is essential - if not present it is almost impossible to inflate the alveoli.

b. Chest injuriesii. Good elastic recoil (promotes expiration)

1. COPD/emphysemaiii. Increased airway resistance occurs with:

1. Asthma2. COPD3. Cystic fibrosis

e. Measuring ventilation: spirometer gives these values. Normals are based on age, height, gender.

i. Tidal volume – air exhaled following passive inhalation – lungs at restii. Vital capacity – maximum amount of air moved – forced inhalation.

iii. Forced vital capacity – just the forced exhalation portioniv. Forced expiratory volume in 1 sec. – amount of air forced out in one secondv. Residual volume – air remaining in lungs following forced expiration

vi. Total lung capacity – total amount of air in the lungs during maximum expansion – vital capacity plus residual volume.

f. Impaired ventilation – blocking of airflow into or out of lungsi. Compression or narrowing of airways

1. Occurs anywhere from nose to alveolia. Common cold, laryngitis, asthma, anaphylaxis, Sinusitis, Acute

pharyngitis, foreign object aspiration, laryngeal edema, tracheal stenosis,

ii. Disruption in neuronal transmissions – 1. CNS depression, head trauma, spinal cord injuries, anesthesia, drug

overdose

III. Diffusion: exchange of O2 and CO2 between lungs and blood at the alveolar capillary junctions.a. Junction consists of simple vascular epithelium – basement membrane – space-

basement membrane – simple alveoli epithelium. b. O2 and CO2 diffuse down the concentration gradient:

i. More O2 in alveoli than in bloodii. More CO2 in blood than in alveoli

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c. Diffusion effectiveness is enhanced by:i. Pressure: amount of gas (O2 or CO2)in the blood – diffusion gradient

ii. Solubility: CO2 is more soluble so it diffuses from blood to alveoli (gas) easily.iii. Membranes: the fact that the alveolar capillary junction has super thin

membranes means the distance the gases must travel is very small.1. This is altered if there is a build-up of fluid (increases the distance the

gas must travel) either a. In the lungs: pneumonia, mucus…b. In the space: pulmonary hypertension forces fluid into the space

between the basement membranes.2. Also the anatomy of the lungs increases surface area. We actually have

about a tennis court of surface area in our lungs.

d. Partial pressure is the measurement of dissolved gas in the blood.i. O2 or CO2 consist of particles that are constantly moving about. When they get

in the serum (blood) this creates a pressure. PaO2 or PaCO2

ii. HbO2 (oxyhemoglobin) is oxygen that is bound to hemoglobin – this is NOT available to the cells (they can only access dissolved O2)

1. Oxygen circulates through the body on hemoglobin (RBCs)2. SaO2 tell us how saturated the hemoglobin molecules are.3. Once saturation is achieved the O2 continues to move back and forth

between being dissolved and moved around by hemoglobin.iii. CO2 moves about in a similar fashion – it is more easily dissolved so doesn’t

need RBCs as much or binds to RBCs as part of bicarb HCO3

e. Impaired diffusion: restriction of the movement of oxygen or carbon dioxide between the alveoli and the blood. Problem occurs with pressure, solubility of gases, or membrane issues:

i. Pressure of oxygen increases with:1. Increase in barometric pressure2. Temperature increase (fever – increases the activity of the molecules)

ii. Pressure of oxygen decreases with:1. Change in altitude (high elevations)2. Hypothermia3. Oxygen deprivation

iii. Membranes:1. Alveoli that are filled with fluid or exudate or mucus lead to increased

distance between air and membrane surfaces.2. Damage to alveoli or capillaries limits the useable surface area.3. Chronic inflammation/damage leads to fibrosis and thickening of the

alveolar capillary membrane.

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IV. Ventilation-perfusion mismatch: V/Q mismatching – this means that either the amount of air (oxygen) or the amount of blood is not sufficient for gas exchange.a. Optimum ventilation-perfusion is almost equal but really means that there is both

oxygen (gas) and blood at the alveolar capillary junctions.b. Mismatches occur:

i. If there is no oxygen but there is perfusion1. Mucus plug, atelectasis, fluid/exudate build up, 2. pulmonary edema – see Lewis table 28-25

ii. If there is no perfusion but there is oxygen1. PE, decreased CO: hemorrhage, MI….

V. Impact of impairment in ventilation and/or diffusion:a. Hypoxemia/Hypoxia

i. Inadequate presence of oxygen reduces the pressure (remember this is needed for it to diffuse into blood and from blood into cells)

1. Due to: hypoventilation, inadequate available oxygen (Mt. Everest)ii. Hypoxia is lack of O2 in cells which leads to anaerobic metabolism and metabolic

acidosis. Cell death results.iii. Brain is super sensitive: restlessness (early sign), lethargy, coma, death

b. Hypercapniai. Again hypoventilation results in build-up of CO2 which lead to respiratory

acidosis. 1. Leads to electrolyte imbalances with alterations in cardiac and brain

function.ii. Air trapping – seen in COPD, Asthma also increases retention of CO2

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VI. General manifestations of impaired ventilation and/or diffusion: Lewis table 26-2a. Cough

i. Fairly common – remember it is a protective mechanism1. Viruses, allergies, aspiration, PE

ii. Chronic – asthma, GERDs, chronic postnasal drainage, chronic bronchitis, lung cancer

b. Excess mucus productioni. Usually inflammatory response – specific pathogens result in differences

1. Bacterial – thick, purulent (pus)2. Pneumococcal – rust-colored, dark3. TB – blood tinged, foamy

c. Hemoptysis

d. Dyspneai. Subjective feeling of shortness of breath (objective is written as use of accessory

muscles…..)1. You may see retractions or pursed lip breathing

ii. Exact mechanism is often not knowniii. Patient may want to sit up or stand or use the tripod position to maximize lung

capacitye. Use of accessory musclesf. Chest pain

i. Can be in the pleural space – sharp, stabbing pain - pleurisy1. Pain increases with deep breath2. Can hear a ‘friction rub’ while listening3. Usually bacterial

ii. Due to inflammation of cartilage, chest wall, intercostal musclesg. Barrel chest – present with chronic lung diseasesh. Adventitious breath sounds –

i. Some indicate the presence of fluid: crackles, ralesii. Some a narrowing of airways: wheezing, rhonchi, stridor

iii. Some the absence of air movement: diminished, absent (atelectasis)

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VII. Systemic manifestations of poor ventilation and/or diffusiona. Cyanosis – desaturated hemoglobin leads to a bluish hue to the bloodb. ABG values – Lewis table 26-1

i. What does PaCO2 tell you – what are normal valuesii. What does PaO2 tell you – what are normal values

iii. What does SaO2 tell you – what are normal valuesc. Mental status

i. Restlessness, lethargy…..d. Finger clubbing

i. Present with chronic ventilation/diffusion issues

VIII. Specific disorders: Why do they cause a problem? What is not working? How do they create a V/Q mismatch?a. Pneumonia - Lewis fig 28-1

i. Red Hepatization versus Gray

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b. COPD: asthma, emphysema, chronic bronchitis

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Emphysema = alveolar issues

Bronchitis=airway obstruction


c.

d. Chest trauma

e. Are there others you can think of?

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Pneumothorax – due to a perforated lung. Pressure increases on injured side, mediastinal displacement leads to both cardiac and respiratory issues.

ARDS

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