Pathophysiology Module 12

Elasticity

The ability to expand and exhale/inhale.

• when everybody takes a deep breath and passively let it out.

True or false: when something comes back to its original shape or position after being stretched (elasticity), it is considered recoil.

True

Compliance

Increased compliance = easy to ventilate a patient

Decreased compliance = stiff lungs → work of breathing is increased

What helps decreased compliance?

Surfactant

What is surfactant?

reduces surface tension within the alveoli allowing for adequate lung expansion for good gas exchange

• helps alveoli remain inflated between breaths

Neuro-chemical control

Central chemoreceptors vs peripheral**

Where are central chemoreceptors located?

The core

What changes stimulate the activation of the central chemoreceptors (CCR)?

Partial pressure of CO2 (PaCO2) & blood pH

• Also sensitive to oxygen

Where are peripheral chemoreceptors located?

The periphery (outside of the core)

What changes stimulate the activation of the peripheral chemoreceptors (PCR)?

Decreased partial pressure of oxygen (PaO2)

What happens if we retain too much CO2?

Acidotic conditions → respiratory acidosis

Where does gas exchange occur?

In the bases of the alveoli.

How do we improve the gas exchange of a patient?

We want to sit the patient up & get them out and walking.

• Naturally breathe better when walking

What occurs in normal circumstances when there are changes to PaCO2 & decreased PaO2?

Triggers activation of central chemoreceptors & peripheral chemoreceptors → triggers brainstem which is the respiratory center of the body (increased breathing) → muscles of breathing get a workout → inhale more oxygen and exert more CO2

Oxygen-Hemoglobin Dissociation Curve

O2 Saturation = above 95%

• If acidotic, O2 cannot bind bc they have hyperkalemia and H+ ion binds to hemoglobin

How many oxygen bind to 1 hemoglobin?

4

What do we see with respiration in the aging adult?

• Decrease in gas exchange

• Decreased elasticity & compliance (stiffer) → hypoxemic & acidotic

• Decreased responsiveness of chemoreceptors → signal to breathe faster in acidotic situations doesn’t work

• Decreased exercise tolerance

• Increased vital capacity & residual volume → hyperinflation due to improper exhalation

Hypercapnia

Increase in PaCO2

• Decreases pH → respiratory acidosis (H+ binds to hemoglobin) → hypoxemia

Hypoxemia

Decreased oxygenation of arterial blood

• NOT O2 saturation

Hypoxia

Decreased O2 saturation in the tissues

What is normal atmospheric oxygen?

21%

• Lessened in high elevations

What causes hypoxemia or hypoxia?

• Decreased inspired O2 → high elevation

• Hypoventilation → slowed breathing → post surgery

• O2 diffusion impaired → goes with acute respiratory distress syndrome → alveoli destruction

• V/Q mismatch → most common

How do we avoid hypoxemia in a patient post surgery?

• Talk to them a lot

• Tell them to take deep breaths

• The more the patient wakes up, the better they breathe.

Clinical manifestations of respiratory difficulty

• Dyspnea (difficulty breathing)

• Breathing pattern (tachypnea vs kussmaul’s vs apnea)

• Cough → wet cough (secretions) & tight cough (narrow from inflammation)

• Hemoptysis → blood in sputum

• Sputum

• Cyanosis

• Pain → pleurisy

• Clubbing → seen in COPD

True or false: green sputum (secretions) indicate a bacterial infection

FALSE → could be bacterial or viral or could have just sat for a while before being coughed out

Normal perfusion for alveolar ventilation

• The heart pumps out 5 liters of blood per min and 4 liters of blood per min can be delivered to the lungs

• Perfusion is greatest at the lung bases

What does V/Q mismatch stand for?

Ventilation / Perfusion mismatch

• Ventilation = getting oxygen in and blowing out CO2

• Perfusion = blood circulation to lungs

Caused by inadequate ventilation of well perfused areas

What is another term for a V/Q mismatch?

Pulmonary Shunts

What is the problem in a right to left shunt?

Ventilation (generally structures within the lung)

• Ex: obstruction of O2 flow to the alveoli

• Ex: inflammation & narrowing of airways caused by asthma

• Ex: pneumothorax

What is the problem in a left to right shunt?

Perfusion (capillaries)

• Overview: oxygen level is okay but not enough blood circulation → compromised perfusion → wasted O2

• Ex: pulmonary embolism

What do we ask patients to do to try to get rid of excess secretions?

We ask the patients to cough to break up the mucus blockages so oxygen can reach the alveoli.

Where do pulmonary embolisms originate from?

• Blood-borne substance lodges in a branch of the pulmonary artery (sepsis)

• Can originate from a deep vein thrombosis

• Fat embolism from femur fracture

• Issue for cancer patients

• Others: thrombus, air (bubble), bone marrow after fx, amniotic fluid

True or false: pulmonary embolisms are found inside of the lungs

FALSE → they are found in the circulation to the lung

Spiral CT

Little pictures are taken of the patient to highlight a pulmonary embolism

Pneumothorax

• Air or gas in the pleural cavity

• Air destroys the negative pressure and the lung collapses

Positive end expiratory pressure

• Negative pressure that prevents lungs from fully collapsing

• -5 cm of water pressure

Can you have gas exchange in a collapsed lung? Will you have breath sounds in a collapsed lung?

No gas exchange in a collapsed lung.

No breath sounds over a pneumothorax.

What are the three types of pneumothorax?

• Open

• Tension

• Spontaneous

Open Pneumothorax

There is an opening to atmospheric pressure (air).

• Ex: trauma → gunshot, car accident, branch through chest

• Ex: chest surgery through chest cavity

If you had to have one of the three types of pneumothorax, which one would you prefer?

Open pneumothorax because when you breathe, you are breathing through the area going out, like a valve opening and shutting.

• CO2 can still be released slightly so the body will not be pressurized as much

Tension Pneumothorax

There are no breath sounds and no air entering or exiting so pressure builds up in the chest and will compress the heart (leading to a code).

• Very bad & must act very fast → chest tubes

• Ex: chest slammed in car accident against steering wheel, broke ribs, 1 rib punctured a lung

If there is a tension pneumothorax in the right lung, how will the trachea appear?

The trachea, instead of being at midline, will shift to the left.

Bleb Pneumothorax

An anatomical weakening of the pleura.

• Can be genetic

• Seen in individuals who smoke

How can mechanical ventilation cause a pneumothorax?

If we set any portion of the mechanical ventilation (ex: tidal volume) too high, then we can cause a pneumothorax for a patient.

• Most at risk: premature babies

What is the treatment for a pneumothorax?

Chest tube → goes in the pleura

• Evacuates air to return negative pressure and inflate the lung

• Typically set to -20

What are the clinical manifestations of pneumothorax?

• Pleural pain

• Tachypnea → uneven chest wall movement

• Dyspnea

• Decreased BP (tamponade)

• Shock (tamponade)

• Decreased breath sounds over area

Atelectasis

The collapse of alveoli (unable to participate in gas exchange).

• Alveoli connect through the Pores of Kohn so if one collapses there is a chain effect

What are the three types of atelectasis?

• Contraction → pulmonary fibrosis

• Absorption

• Compression

Absorption (Resorption) Atelectasis

If there is a collapse of alveoli, gas exchange is inhibited across the Pores of Kohn.

• The alveoli are filled with gunk (mucus or exudate)

• Chain reaction of collapsing alveoli through the pores of Kohn.

• Most common

• Ex: seen in patients who do not receive enough O2 post surgery

Compression Atelectasis

• THINK TUMOR (lung tumor)

• If a tumor compresses on the lung, that region will be unable to participate in gas exchange.

• Ex: pneumothorax or pleural effusion → something is preventing the lung from fully expanding

What are the causes of atelectasis?

• Shallow breathing → waking up from surgery, pain

• Viscous secretions → thick & hard to cough out; they act as a pulmonary clot

What are the clinical manifestations of atelectasis?

• Dyspnea → SOB (chemoreceptors alter respiration)

• Cough → increases negative pressure

• Fever

• Leukocytosis

How do we prevent atelectasis?

• Cough → increase pressure & removes secretions

• Deep breath → collateral circulation thru pores of Kohn opens up collapsed alveoli

Pleural Effusion

Buildup of fluid in the pleural space

• Increased pressure can cause compression atelectasis

• Very common

What are the three types of pleural effusion?

• Transudate

• Exudative

• Hemothorax

Transudate Pleural Effusion

• Watery fluid

• Congestive heart failure, liver & kidney failure

Exudative Pleural Effusion

• WBC’s & plasma proteins

• Caused by inflammation, infection, & cancer

• Ex: pneumonia

Hemothorax Pleural Effusion

• Blood in the pleural cavity

• Seen in trauma situations → tension pneumothorax

What are the clinical manifestations of pleural effusion?

• Dyspnea

• Compression atelectasis

• Impaired ventilation

• Pleural friction rub

How do we evaluate a pleural effusion?

• CXR → chest x-ray

• Thoracentesis

• Sputum

What are the obstructive airway disorders?

• Asthma

• COPD → chronic bronchitis & emphysema

True or false: chronic obstructive airway disorders are a left to right shunt.

FALSE → they are a right to left shunt because they are impacting ventilation

Bronchial Asthma

• Acute

• Reversible

• Intermittent

Chronic Obstructive Pulmonary Disease (COPD)

• Chronic bronchitis (inflammation of bronchi by irritants) & emphysema together (lost elasticity)

• Irreversible

• 4th leading cause of death

• Most preventable → #1 cause is smoking

• Burns out central chemoreceptors bc baseline for PaCO2 is 65 instead of 35-45 → relies on peripheral chemoreceptors (lowered O2)

Asthma

Inflammation with hyper responsiveness of the upper airway & causes bronchospasms

• Typically genetic (intrinsic) or environmental (allergens)

What are the risk factors for asthma?

• Family history

• Allergens

• Urban

• Air pollution

• Smoke

• Recurrent viral infection

True or false: we are seeing a large increase in the number of asthmatics.

TRUE → mainly air pollution

Atopic / Extrinsic Asthma

• Most common (70-80%)

• Low concentration of allergen trigger

  • Type I hypersensitivity reaction

  • First exposure = mast cells sensitized by IgE

Non-Atopic / Intrinsic Asthma

• Mainly seen in adults (very severe in kids)

• Triggers: infection, drugs, cold

• Bronchospasms → imbalance of sympathetic & parasympathetic system

What are the two ways that asthma can present (time-frame)?

• Slow-onset → hours to days

• Hyper-acute → 10 to 20 min after exposure

  • Can progress to Status Asthmaticus (doesn’t respond to treatment & is severe)

Why do we see hypoxemia in asthma patients?

The inflammation leads to..

• Tachycardia

• Increased restlessness

• Tachypnea

What are the clinical manifestations of asthma?

• Cough

• Increased mucus

• SOB

• Wheezing & prolonged expiration

• Increased CO2 retention

• Chest tightness

• Retractions

What is the difference between bronchitis and asthma?

Bronchitis is inflammation of the airways caused by irritants.

Asthma is inflammation of the airways caused by allergens.

Chronic Bronchitis - Pathophysiology

Tobacco → inflammation bc its irritant & foreign → damages airway epithelium → sets off inflammatory process → increased workload → muscle weakness & weight loss → bronchial obstruction/constriction → same symptoms as asthma (dyspnea, cough, increased CO2)

Exacerbation of COPD

• Considered a crisis

• Patient’s oxygen plummets and their CO2 climbs

What happens when you feed a high level of oxygen (40-50%) to a COPD patient?

They immediately stop breathing (apneic).

• Giving them oxygen stimulates the peripheral chemoreceptors to stop causing their respirations as they believe the patient is back to normal

True or false: a COPD patient with very low oxygen levels should receive a 100% O2 mask.

FALSE → this will cause them to stop breathing as the peripheral chemoreceptors won’t stimulate respirations.

Emphysema

• Primary: autosomal recessive → a1-antitrypsin deficit (protects elastin)

• Secondary: decreased body stores of a1-antitrypsin from smoking; 20% of all smokers

What is the primary cause for the development of emphysema?

A lack of A1-antitrypsin

• This prevents lungs from being elastic so there is a loss of recoil → decline in oxygenation

Pathophysiology of emphysema

Lack of A1-antitrypsin → elastin breakdown caused by protease → no lung recoil → emphysema → air trapping / impaired gas exchange → hypoxemia / dyspnea / cough

What are the alterations to structures of the lungs in emphysema?

• Abnormal permanent enlargement of acini

• Destruction on alveolar wall & capillary bed

What is emphysema secondary to?

Chronic bronchitis & smoking

S/S of emphysema

• anterior-posterior diameter increases → barrel chest

• pink puffer → loss of ventilation & perfusion

• pursed lip breathing → improves gas exchange

S/S of chronic bronchitis

• Blue bloaters → hypoxemia & hypercapnia

• exercise intolerance

• labored breathing

Common cold

Viral infection of the upper respiratory tract

• Main spreader: fingers → most people cough in their hands

  • Contaminated surfaces

• Main carrier: young kids; daycare/schools

• Self-limited to about 10 days

What are the types of viruses associated with the common cold?

• Rhinoviruses

• Parainfluenza viruses

• Respiratory syncytial virus

• Coronaviruses

• Adenoviruses

How many colds per year is common?

2-3

What are the signs and symptoms of the common cold?

• sore and scratchy throat followed by profuse and watery rhinorrhea

• nasal congestion

• sneezing

• coughing

• General virus symptoms: malaise, fatigue, headache, myalgia (muscle pain)

Rhinosinusitis

Inflammation of the nasal passage & paranasal sinuses.

• Generally connected to viral infection & allergies

• Obstruction of the narrow ostia that drains the sinuses → impairment of mucociliary clearance

• Acute = 5-7 days (viral); <4 weeks (bacterial)

• Subacute = 4-12 weeks

• Chronic = > 12 weeks

Why is mucus important?

Traps antigens.

If a patient came to you and only complained of tenderness in their maxillary sinuses, what should we consider?

Tooth infection or abscess

What are the signs and symptoms of rhinosinusitis?

• facial pain / headache

• purulent nasal discharge

• decreased sense of smell

• fever → differs from common cold

What is purulent discharge?

A thick, milky discharge.

What are the chronic signs and symptoms of rhinosinusitis?

• sense of fullness in the ears, postnasal drip, hoarseness, chronic cough, loss of taste & smell

• absence of pain

• intracranial & orbital wall complications → if not treated

Influenza

• Most common cause of infection

• Mainly occurs from October-March; peak in February

How many deaths occur per year due to influenza?

35,000 deaths (range is 15,000 - 85,000)

Why did influenza deaths go down in the year 2021?

Everyone was being diagnosed with COVID

Why is influenza’s peak in the winter and drop off in the summer?

The influenza virus survives longer in colder temperatures.

Why is a fever associated with influenza?

A fever occurs in patients with influenza because the body is attempting to raise the internal core temperature to kill the virus as it survives longer in cold temperatures.

What family does influenza viruses belong to?

The orthomyxoviridae family