hsc4555 ucf dr.ferdowsi exam 3

Respiratory system divided into

Upper/Lower airway

Treatment of acute respiratory distress syndrome

Mostly supportive

Enhance tissue oxygenation until inflammation resolves

Identify underlying cause (ex: sepsis)

Maintain fluid and electrolyte balance

Increased fluid administration can

produce or intensify pulmonary edema

Block system inflammatory cells

Adequate oxygenation

Upper airway

nasopharynx

oropharynx

laryngopharynx

Lower airway

larynx

trachea

bronchi

bronchopulmonary segments

terminal bronchioles

acinus

Nasal cavity structure

rigid box:

1/3 bone

2/3 cartilage

prevents collapse of nose during air movements

Highly vascular mucosa

Vibrissae

large hairs that filter air in the nose

nasal cavity functions

Gas exchange system

primary function

Heat exchange system

brings air to body temp

cilia

filter air and mucus

epithelial lining of trachea and bronchi

Pseudostratified ciliated columnar epithelium

Goblet cells

produce mucus

Mucus composed of

95% water 5% mucopolysaccharides, mucoproteins and lipids

Ciliary function impaired by

Smoking, alcohol

extreme temps

Low humidity

starvation

anesthetic, corticosteroids, noxious gases

Common cold

effect of mucus production on ciliary function

increased mucus production decreases ciliary function by sticking cilia together and preventing movement

Conducting airways

Trachea, bronchi, and bronchioles

no gas exchange

Respiratory bronchioles

where gas exchange begins

bronchopulmonary segments

terminal bronchioles

respiratory bronchi

alveoli

Type II alveolar cells

produce surfactant

Type I alveolar cells

Where most gas exchange

occurs

Alveolar macrophages

phagocytose small particles in alveoli

Autonomic nervous system control of lower airways

Control bronchi and bronchiole musculature

Sympathetic stimulation of lower airways

mediated by β2-adrenergic receptors

relaxation of muscle

Parasympathetic stimulation of lower airways

mediated by acetylcholine receptors

via the Vagus (CNX) nerve constriction of muscle

Blood supply in Pulmonary Circulation

Blood supply from two sources:

Bronchial arteries

Pulmonary arteries

Bronchial arteries

provide oxygenated blood to lung tissue

Pulmonary arteries

the vessels that carry deoxygenated blood to lungs for gas exchange

Pulmonary venous blood

oxygenated

Ventilation

movement of air in and out of the lungs

Dead Space

3 kinds

anatomic

alveolar

physiologic

Anatomic dead space

volume of gas not used in gas exchange

Alveolar dead space is aka

wasted ventilation

Alveolar dead space

ventilated, but unperfused / underperfused alveoli

Physiologic dead space

sum of anatomic and alveolar dead spaces

Physiologic dead space is aka

functional dead space

Mechanisms of Breathing During inspiration

chest wall muscles contract

diaphragm moves downward

creating a negative intrapleural pressure

causing air to flow into lungs

Surfactant

decreases surface tension, allowing the alveoli to open easily with each breath.

Lack of surfactant can result in

alveoli collapse

atelectasis

alveoli collapse

Mechanisms of Breathing During Expiration

lung deflates b/c they have recoil tendency

relaxation of the diaphragm

air flows out

functional residual capacity

volume of air remaining in the alveoli after gas exchange

Factors Affecting Breathing

Airway Resistance

Lung Compliance

Distribution of Ventilation

Neurological control of ventilation

airway resistance

Relationship between pressure and flow

airway resistance calculation

Resistance = Diving Pressure ÷ Rate of flow

Resistance influenced by

airway radius

pattern of gas flow

airway radius reduced by

Mucus

Bronchospasm

Stress

pulmonary deconditioning

age

Highest airway resistance at the nose

because of turbulent flow and high velocity

Lowest airway resistance is in

small bronchioles,

where turbulent flow is small

Airway resistance is higher in

the neonate rather than the adult

Lung Compliance

Represents lung expandability and ease of lung inflation

Lung Compliance formula

change in volume/change in pressure

Lung Compliance provides

an estimate of airway resistance and elasticity of the lung

Lung compliance increased in

neonates and young children

Lung compliance decreased in elderly because of

increased chest wall rigidity

Reduced mobility of the ribs

Partial contraction of inspiratory muscles

Loss of elastic fibers in the lung

diseases that can affect lung compliance

cystic Fibrosis, Hydrothorax

Distribution of Ventilation

Affected by position

Alveoli are larger in

the apices of the upright lung than in the base

Ventilation increased in

the bottom of the upright lung

In the supine lateral position

ventilation is best in the dependent part of the lung fields

Neurologic Control of Ventilation

pons and medulla oblongata

respiratory center

pons and medulla oblongata

Efferent fibers travel from the brainstem to

diaphragm via phrenic nerve to stimulate inspiratory muscles

Medullary dorsal neurons stimulate

inspiratory muscles (intercostals, diaphragm)

Abrupt cessation of neurostimulation allows for

expiration

Pneumotaxic center

Located in the upper pons

Influences rate of respiration

Ends inspiration

Central chemoreceptors

Located in the medullary center

Responds to changes in CO2 and pH

Peripheral chemoreceptors

Located in the aortic arch and carotid bodies

Respond to decrease in arterial O2

All hypoxemia is

b/c hypoxia but not all hypoxia causes hypoxemia

Baroreceptors

Located in aortic arch and carotid arteries

Respond to changes in B/P

increased blood pressure causes

respiration to decrease

decreased blood pressure causes

respiration to increase

Hypoventilation

Air delivered to alveoli is insufficient to provide O2 and remove CO2

Hypoventilation results in

increased PaCO2 and hypoxemia

Causes of hypoventilation

Drugs: morphine, barbiturates

obesity

Disease: myasthenia gravis, obstructive sleep apnea, chest wall damage, paralysis of respiratory muscles,

Iatrogenic: surgery of the thorax or abdomen

Hyperventilation

excess of air entering the alveoli

Hyperventilation results in

hypocapnia

hypocapnia

insufficient carbon dioxide

Causes of hyperventilation

pain,

fever,

anxiety,

obstructive and restrictive lung diseases,

sepsis,

high altitude

brainstem injury

Low PaCO2 leads to

greater binding of oxygen to the hemoglobin molecule

Obstructive Pulmonary Disorders manifest by

increased resistance to airflow

asthma Obstruction indicated by

FEV1/FVC < 75%

Classifications of Obstructive Pulmonary Disorders

from conditions in the wall of the lumen

related to loss of lung parenchyma

Obstruction of the airway lumen

Obstruction from conditions in the wall of the lumen

Asthma

Acute Bronchitis

Chronic Bronchitis

Obstruction related to loss of lung parenchyma

Emphysema

lung parenchyma

portion of the lung involved in gas transfer

Obstruction of the airway lumen

Bronchiectasis

Bronciolitis

Cystic Fibrosis

Acute Tracheobronchial

Obstruction

Epiglotitis

Croup Syndrome

Asthma

Occurs in 7% to 14% of U.S. population

Most common chronic disease of children

Asthma Characterized by

Airway obstruction that is reversible(in most pts)

Airway inflammation

Increased airway responsiveness to a variety of stimuli

Asthma High-risk populations

African Americans

Inner-city residents

Premature/low-birth-weight children

Asthma Predisposing factors

Genetics (strongest factor)

History of hay fever, eczema

Family history

Positive skin test reactions to allergens

Asthma genetics

atopy (Chromosomes 5, 11, 14)

structural (smaller airways)

Asthma types

intrinsic and extrinsic

intrinsic asthma

non-allergic, adult onset

Develops in middle age

No history of allergies

Respiratory infections or psychological factors related

extrinsic asthma

allergic, pediatric onset

1/3 to 1/2 of asthma cases

An IgE-mediated response is common

Exercise-induced asthma

Common in children and adolescents

Bronchospasm often occurs within 3 minutes after the end of exercise; usually resolves in 60 minutes.

Heat loss, water loss, and increased osmolarity of the lower respiratory mucosa stimulate mediator release from basophils and tissue mast cells

mediator released during Exercise-induced asthma causes

bronchospasm

Other causes of asthma

Occupational

Drug-induced

food additives

Gastroesophageal reflux disease

Immunohistopathologic features of asthma

- Denudation (loss of outside layer) of airway epithelium

- Collagen deposition beneath the basement membrane

- Edema

- Mast cell activation

- Inflammatory cell infiltration by neutrophils, eosinophils, and lymphocytes

Inflammation of the airway of asthma

Acute bronchospasm (bronchoconstriction)

Mucosal edema, mucus plug formation

Airway wall remodeling: thickening of basement membrane

clinical manifestations of asthma

Wheezing

Feeling of tightness of chest

Dyspnea

Cough

Hyperinflated chest

Decreased breath sounds

Tachycardia

Earliest sign of exacerbation of asthma

Cough (dry or productive)

Increased sputum (coughed up mucus) production (thick, tenacious, scant, and viscid

Clinical manifestations of severe asthma attack

Use of accessory muscles of respiration

Intercostal retractions

Distant breath sounds with inspiratory wheezing

Orthopnea (dyspnea that occurs when lying flat)

Agitation

Tachypnea:

Tachycardia

PEFR: <80 L/min