Pathophysiology 1 - Chapter 21

Upper Airway Structures

• Nasopharynx

• Oropharynx

• Laryngopharynx

Lower Airway Structures

• Larynx

• Trachea

• Bronchi

• Bronchioles

• Alveoli

Vibrissae function

Large hairs that filter air in the nose

Describe Cilia

Sweep foreign particles and mucus upward to be swallowed or expectorated

When ciliary function gets impaired by smoking, alcohol, hypothermia, cold air, low humidity, starvation, anesthetic, corticosteroids, noxious gases, the common cold what happens?

mucus production increases

Conducting airways

• trachea

• bronchi

• bronchioles

Does gas exchange happen in conducting airways?

No, only in alveolis

Bronchi

Made out of cartilage and smooth muscle

Each segment divides into

50+ terminal bronchioles

Main bronchi divides into

lobar branches

Lobar branches divide into

Bronchiopulmonary segments

Terminal bronchioles subdivide into

two or more respiratory bronchioles

Respiratory bronchioles is where

Gas exchange begins

Respiratory bronchioles divide into

Two or more alveolar ducts which serve several alveoli

Gas exchange occurs in

Alveolar units

Grape like structure of alveoli provides

A huge surface area for gas exchange

Adult lungs contain how many alveoli?

~300 million alveoli

Newborn contains how many alveolis?

~1/8 of adult alveolis

3 structures of one alveoli

• alveolar macrophages

• type I alveolar cells

• type II alveolar cells

Alveolar macrophages

Phagocytose foreign particles (immune cells)

• those damaged by smoking and inhalation of silica

Type I alveolar cells

Epithelial structural cells

• also called pneumocytes

Type II alveolar cells

Produce surfactant

• phospholipid that lowers surface tension

• facilitates gas exchange

Surfactant prevents

Alveolar walls from collapsing

Partial pressure of gases in alveoli:

• PAO₂ for oxygen

• PACO₂ for carbon dioxide

Partial pressure of gases in the blood:

• PaO₂

• PaCO₂

Collateral ventilation happens through

Pores of Kohn or canals of Lambert

Blood supply to the lungs comes from two sources:

• bronchial arteries

• pulmonary arteries

Bronchial arteries

Supply small amount of oxygenated blood to pleura and lung tissues

• feed cells

Pulmonary arteries

Vast network of capillaries that provides for gas exchange

• participates in gas exchange

Capillary networks less in

neonate, young children, and elderly

Blood from right ventricle goes to pulmonary arteries (unoxygenated) and then to

Pulmonary arterioles to the capillary membrane for gas exchange

Ventilation is the process of

moving air into the lungs and distributing air to the alveoli for maintenance of oxygenation and removal of CO₂

Tidal volume

Amount of air entering the lung after a normal breath ~500 mL

Inspiratory reserve volume

amount of air a person is able to inspire above tidal volume ~3.0 L

Expiratory reserve volume

amount of gas expired beyond tidal volume ~1.2 L

Residual volume

volume of gas left in lungs at the end of maximal expiration ~1.2 L

Vital capacity

volume of gas that can be exhaled during maximal expiration ~4.8 L

Inspiratory capacity

amount of gas that can be inspired from a resting expiration ~3.5 L

Functional residual capacity

amount of gas left in lungs at the end of normal expiration ~2.4 L

Total lung capacity

amount of gas contained in lungs after maximal inspiration ~6 L

During inspiration

Chest wall muscles contracts, elevating the ribs as the diaphragm moves downward, creating a negative intrapleural pressure

During expiration

lung deflates passively because of elastic recoil and relaxation of the diaphragm

Surfactant decreases surface tension meaning

it allows the alveoli to open easily with each breath

• lack of surfactant can cause the alveoli to collapse - atelectasis

Airways and tissues in the lungs resist

inflationR

Resistance in the lungs are provided by the

• radius of airways: the smaller the radius, the more resistance

• elastic fibers

• surface tension in the alveoli

Highest airway resistance is where

The nose because of turbulent flow and high velocity

Lowest airway resistance is where

the small bronchioles

• innervated by autonomic nervous system

Neural control centers

• Nerve impulses stimulate muscles in the diapragm

• Cessation of impulses allows for expiration

• Pneumotaxic center (in pons) influences respiration rate

Chemoreceptors

• Central (located in the pons) and peripheral (located in the aorta and carotid artery)

• responds to changes in arterial CO₂ and pH

Lung receptors

• Inflation of the lung send impulses via the vagus nerve to the medulla to cause inhibition of inspiration

Proprioceptors (located in muscles, tendons, joints)

• Body movement leads to stimulation of respiration

Baroreceptors (located in the aorta and carotid artery)

• respond to changes in blood pressures

• increase in arterial blood pressure leads to inhibition of respiration

*Perfusion

Is it well circulated by capillaries?

With a shunt, deoxygenated blood cannot get reoxygenated because

there is no oxygen in the alveolus so it goes right through

Poorly ventilated alveoli

• Obstructed airway path

• Causes less O₂ to alveoli = capillary doesn’t get O₂, more CO₂ left over

Poorly perfused alveoli

• No blood supply to alveoli

  • Pulmonary semilumar valve stenosis

  • Pulmonary Embolism

  • Right sided heart failure

• Can become ischemic

Shunt in alveoli

• Alveoli not able to open up (not ventilated)

How long does it take for O₂/CO₂ to perform gas exchange at alveoli?

~0.25 seconds

Causes of impaired diffusion

• thickening of the alveolar-capillary membrane

• decreased available surface area

• increased physical activity

• mismatch between perfusion and ventilation

• elderly and newborn

Hypoventilation

• occurs when air delivered to alveoli is insufficient to provide O₂ and remove CO₂

• results in high PaCO₂ in blood stream (>45 mmHg), hypercapnia, and hypoxemia

Causes of hypoventilation

• morphine

• barbiturates

• obesity

• myasthenia gravis (weakness in muscles for breathing)

• obstructive sleep apnea

• chest wall damage, paralysis of respiratory muscles

• surgery of the thorax or abdomen

Hyperventilation

• increase of air entering the alveoli leads to hypocapnia (PaCO₂ <35 mmHg)

Hyperventilation causes

• hypoxic stimulation of peropheral chemoreceptors

• pain

• fever

• stress

• anxiety

• high altitude

• obstructive and restrictive lung diseases

• sepsis

• brainstem injury

less common causes = bolded

Obstructive pulmonary diseases

• caused by increased airway resistance as a result of:

  • plugging of airways from increased sputum production

  • mucosal hypertrophy and edemma (commonly in elders)

  • loss of structural integrity of the airway

  • airway narrowing from bronchial smooth muscle contraction, when there is hyperactivity of the airways

• example: asthma

Hypoxemia

Deficient blood oxygen as measured by low arterial O₂ and low hemoglobin saturation

Hypoxia

A decrease in tissue oxygenated

Types of Hypoxia

• hypoxic hypoxia

• anemic hypoxia

• circulatory hypoxia

• histotoxic hypoxia

Hypoxic hypoxia

high altitude, hypoventilation, obstruction

Anemic hypoxia

due to low hemoglobin

Circulatory hypoxia

due to low cardiac output; shock

Histotoxic hypoxia

decreased O₂, carrying capacity from toxic substance, cyanotic poisoning

Acute Respiratory Failure (ARF)

• Stage of disturbed gas exchange resulting in

  • low PaO₂

  • high PaCO₂

  • pH less than 7.30

  • when patient breathing room air

Three categories of ARF

• failure of respiration or oxygenation leading to hypoxemia and normal or low carbon dioxide levels

• failure of ventilation leading to hypercapnia

• combination of respiratory and ventilatory failure

ARF Etiology

Depends on the cause

• central nervous system problems

• neuromuscular diseases

• chest wall and diaphragm dysfunction

• pulmonary parenchyal diseases

  • tissue and space around alveoli

• airway problems (ex. asthma)

ARF Clinical Manifestations early on

rapid, shallow breathing

ARF Clinical Manifestations late

cyanosis, nasal flaring

Pulmonary Hypertension (HTN)

• Normally, pulmonary circulation is high flow and low pressure

• Sustained pulmonary artery systolic pressure >25 mmHg resting and >30 mmHg with exercise

Primary (idiopathic) pulmonary HTN

• rare

• rapidly progressive and occurs more often in women

• long-term prognosis is poor and medical treatment is usually ineffective

Secondary pulmonary HTN

• from a known disease

• three mechanisms

  • increased pulmonary blood flow

  • increased resistance to blood flow (most common and usually due to hypoxic vasoconstriction, eg: chronic bronchitis)

  • increased left atrial pressures

Pathogenesis of pulmonary hypertension

Initially walls of small pulmonary vessels thicken from an increase in the muscle; internal layer of pulmonary artery wall becomes fibrotic

• this occurs as a result of local tissue hypoxia

Sustained pulmonary hypertension results in

Formation of a network of blood vessel lesions (plexiform) that impede blood flow

Pulmonary hypertension treatment

• treat underlying cause

• supplemental oxygen

• vasodilators

• diuretics

• in advanced cases: lung or heart-lung transplant

• left to right shunts (surgery)

Pulmonary embolus

An undissolved detached material (ex: blood clot, fat emboli, air, tumor) that occludes blood vessels

• 90% of emboli are clots that originate in deep veins of lower extremeties

3 main factors of Virchow’s Triad that causes thrombus formation

• Venous stasis/sluggish blood flow

• Hyper coagulability

• Damage to venous wall (intimal injury)

Pathogenesis of Pulmonary Venous Embolism

Thrombus dislodged from point of origin by:

• direct trauma

• exercise

• muscle action

• changes in blood flow

What lobes are frequently involved in pulmonary venous embolism

Lower lobes frequently because of higher blood flow

Venous occlusion (>25-30% of vessels) causes a ___ in pulmonary artery pressure and potential ___-sided heart failure which leads to hypotension

rise; right

True or False: Actual pulmonary infarction (death of lung tissue) may or may not occur

True

Four major types of pulmonary malignancies

• large cell carcinoma

• small cell carcinoma

• squamous cell carcinoma

• adenocarcinoma

Large cell carcinoma

develop in the periphery

Small cell carcinoma

central bronchial region; fastest growing

Squamous cell carcinoma

central bronchial region

Adenocarcinoma

most common, in the peripheral lung

Clinical manifestations of pulmonary malignancies

• depends on type and location of tumor

• can be asymptomatic

• signs and symptoms can be classified as intrathoracic or extrathoracic

Intrathoracic manifestations

• dyspnea

• cough

• chest pain

• hemoptysis

• hoarseness

• increased sputum

Extrathoracic manifestations

• weight loss

• fatigue

• anorexia

• anemia

• clubbing of nails

• facial and upper extremity edema (superior vena cava syndrome)