Cardio WEEK 1-2

Describe the difference between obstructive and restrictive lung disease

Obstructive:

Airway obstruction causes an increasin resistance to airflow, particularly during exhalation. "Hard to exhale from the lungs"

Restrictive:

Compliance of the lungs is reduced, increasing lung stiffness, limits inspiratory expansion, reducing lung volumes. "Hard to fully expand. Hard to get air in."

What are examples of obstructive lung diseases? Restrictive?

Obstructive:

- Chronic obstructive pulmonary disease (COPD)

- Bronhiectasis

- Cystic fibrosis

- Asthma

Restrictive

- Interstitial lung disease (ILD)

- idiopathic pulmonary fibrosis (IPF)

- Sarcoidosis

- Obesity

- Scoliosis

- Neuromuscular disease

What are PFTs? What are they used for?

Pulmonary Functional Tests;

- monitor pt with known respiratory disease

- guide decisions regarding further treatment and interventions

List 3 PFTs

- Spirometry

- Body plethysmography

- diffucion capacity of carbon monoxide (DLCO)

What does spirometry measure

volumetric flow rate (volume agasint time) "How much air and how fast"

What two curves can be gernerated from spirometry readings

- volume-time curve

- flow-volume curve

Two instructions for pt about to perform spirometry

1. maximal inspiration

2. forcefully exhale as quickly as possible and for as long as possible

Three measurements collected from volume-time curve include

- Forced expiratory volume in one second (FEV1)

- Forced vital capacity (FVC)

- Ration of FEV1/FVC

What is FVC and how is it calculated

Forced vital capacity; the total volume that can be forcefully expelled from the lungs

FVC = IR + ER + TV

Initial steep portion of the FV loop reflects what

Large airway function

Expiration is -ve or +ve on the FV Loop

+ve

What TLC? How is it calculated

Total lung capacity; the maximum colume of air the lungs can hold after a full, deep inhalation.

TLC = FVC + RV

or = IR + ER + TV +RV

What is RV

Resdual volume; the amound of air remaining in the lungs after a maximal exhalation, which cannot be voluntairly expelled

The right most point on the FV loop represents what? The left most represents what? What is the difference between these points?

Right: RV

Left: TLC

Difference: FVC

Why does RV appear to have a greater volume than TLC on the FV Loop?

x-axis represents expired volume of air. The points of RV and TLC are the points at which they exist within the lungs during the breath cycle, they are are not the volumes displayed on the plot.

Following peak expiratory flow on the FV loop, what drives expiration

Largely independent of the driving force (effort) and is instead limited by the mechanical properties of the lungs;

- airway compression: forceful expiraitio ncauses airway compression, which increases airwat resistance

- reduced radial traction: as lung volume decreases, the radial traction exerted by the lung parenchyma on the airways also declines, causing them to become smaller and limiting flow

What is radial traction

the result of alveolar expansion, pulling open the airways due to the parenchymal fibers attached to the alveoli and the exterior of the airways. This decreases airway resistance as lung volume increases. (larger alveoli have less resistance)

What does body plethysmography measure

Static lung volume; "how much air"

Compare lung volumes and capacities

Volumes:

How much air the lungs can hold or move at different stages of ventilation

Capacity:

Combinations of volumes that descrribe the functional capacity of the lungs

What is IC? How is IC calculated?

Inspiratory Capacity; max air you can inhale after a normal TV exhalation

IC = VT + IRV

What is FRC? How is FRC calculated?

Fucntional Residual Capacity; air remaining in the lungs after a normal TV exhalation

FRC = ERV + RV

Clinical significance of FRC

- keeps small airways open to prevent alveolar collapse

- keep a volume of air in the lungs at end expiration to facilitate gas exchage

* Can be affected by disease*

Clinical significance of RV

Prevents lung collapse at end of forced expiration (keeps alveoli inflated)

What does diffusion capacity of the lung for carbon monoxide (DLCO) measure

How well gas is being exchanged at alveolar-capillary membrane. "How effective is gas exchange?"

What would a low DLCO signify

impaired gas exchange - O2 can't easily move from the alveoli to the blood

Compare changes to the spirometry volume-time curve in obstructive and restrictive diseases.

Obstructive:

Obstruction to expiratoy airflow leads to shallow exhalation curve and so;

- low FEV1

- FEV unchanged

- FEV1/FEV decreased (<0.8)

Restrictive:

Restriction decreases lung volumes but expiratory airflow is preserved.

- low FEV 1

- low FEV

- FEV1/FEV remains normal

Compare changes to the spirometry flow-volume curve in obstructive and restrictive diseases.

Obstructive:

- decereased peak expiratory flow

- "scooping" or "coving" , concavity of the curve marks reduction in expiratory flow in obstructive disease

Restrictive:

- Shape of curve maintained, scaled down due to reduced overall volumes

Explain why we see the changes to flow-volume curve in obstructive and restrictive diseases.

Obstructive:

Airflow limited during expiration when the airways cannot stay open; Obstruction due to

- Narrowing (mucus/secretions. bronchoconstriction)

- Prone to collapse (due to reduced airway support)

- Lacking radia traction (from surrounding lung tissue such as in emphysema)

Restrictive:

Altered due to limitation in lung expansion (compliance); overall reduction in lung volumes

How do lung volumes change in restrictive vs. obstructive disease (IRV, TV, ERV, RV, TLC, FRC)

Restrictive:

- IRV low

- TV low

- ERV low

- RV low

- TLC decreased; hallmark of restrictive disease

- FRC may be unchanged buy typically decreased

Obstructive:

- IRV very low

- TV normal

- ERV high

- RV very high

- TLC normal or increased; severe obstruction can cause hyperinflation

- FRC increased due to air trapping (high RV and ERV)

*Increased FRC makes it hard to take in air on subsequent inspiratory effort**

How do DLCO scores change in obstructive vs. restrictive diseases

Obstructive:

- normal or mildly decreased (diffusion capacity not compromised in inital stages of disease)

- severe cases, DLCO can significantly reduce if there is significant damage to alveolar capillary membrane or vascular structures

Restrictive

- decreased DLCO (often)

- some conditions (interstitial lung disease) lead to damage or thickening of alveolar-capillary membrane, reducing the efficiency of gas exchange

**Shortness of breath due to limited O2 diffusion, leads to rapid desaturation with increased O2 demand in exercise

COPD

Chronic Obstructive Pulmonary Disease is a preventable and treatable disease characterized by airflow limitations that is not fully reversible.

What causese the air flow limitation in COPD

Airflow limitations is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoke.

TF COPD only affects the lungs

F - Although it affects the lungs, COPD also produces significant systemic consequences

TF COPD has a significant genetic component

T - for people with aplpha-1 antitrypsin deficiency, a protein made in the liver that protects the lungs from inflammation-related damage

What are the 7 classifications of COPD (ACID PUG)

1. Genetically determined (COPD-G)

2. Developmental abnormalities in the lung (COPD-D)

3. Cigarette Smoke (COPD-C)

4. Pollutants or biomass exposure (COPD-P)

5. Infection (COPD-I)

6 Asthma (COPD-A)

7. Uknown cause (COPD-U)

Explain pink puffer phys/blue bloater bronc

Pink Puffer

- Typical disease: Emphysema-predominant COPD

- Appearance: Thin, weight loss

- Breathing: Severe shortness of breath, pursed-lip breathing ("puffing")

- Oxygen: Relatively preserved → "pink"

- CO₂: Normal or low (not retaining CO₂)

Blue Bloater

- Typical disease: Chronic bronchitis-predominant COPD

- Appearance: Overweight, edematous ("bloated")

- Breathing: Chronic productive cough

- Oxygen: Poor → cyanosis ("blue")

- CO₂: Elevated (CO₂ retention), prone to right-heart failure

Emphysema

Defined pathologically as the presence of permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied be destruction of their walls and without obvious fibrosis

Chronic bronchitis

Defined clinically as chronic productive cough for 3 months in each of 2 successive years in a pt. in whom other causes of productive chronic cough have been excluded

What are the two phenotypes at high risk of COPD

COPD frequent sxacerbator phenotype:

pt with two or more exacerbations annually

Inflammatory phenotype:

ptwith persistently elevated serum concentrations of inflammatory markers. (eosinophilic/neutrophilic)

Signs and symptoms of COPD

- persistent cough and sputum

- frequent respiratory tract infecitons

- progressive activity-related shorness of breath (dyspnea) with resultant activity limitation

Why is COPD diagnosis limited?

pt don't complain until symptoms get severe + up to 4 year wait for diagnostic spirometry

Pathophysiology: What lung structures are affected by COPD

Narrowing of;

- central airway

- peripheral airways

- parenchyma (resp. bronchioles, alveoli, capillaries)

- vasculature

Explain the effect of emphysema on radial traction

- Chronic inflammation releases enzymes (neutrophils) that degrade elastin in the elastic fibers of the parenchyma allowing airways to collapse more readily against positive expiratory pressure

- neutrophils also break down alveolar wall, reducing surface area for gas diffusion

What is the equal pressure point theory

- During forced expiration, pressure inside the airways decreases as air flows toward the mouth.

- At some point, airway pressure equals pleural pressure → this is the equal pressure point.

- Beyond this point (toward the mouth), pleural pressure exceeds airway pressure, causing airway compression.

Explain the effect of emphysema on equal pressure point

- Loss of elastic recoil shifts the EPP deeper into smaller, unsupported airways.

- This leads to dynamic airway collapse and air trapping.

What four results of obstructive lung disease lead to hyperinflation

1. increased compliance of lung tissue

2. decreased airway tethering (radial traction)

3. deacreaed expiratory flow

4. prematire airway closure

Hyperinflation is the result of an increased what?

End Expiratory Lung Volume (EELV) due to excessive air trapping

What is diminished when EELV is elevated? How does this appear on a CXR

Zone of apposition is deminished appearing as a depressed diaphragm on a CXR

Explain intercostal indwelling with COPD

1. Marked negative intrathoracic pressure

- Due to airflow obstruction and hyperinflation, patients must generate greater inspiratory effort.

- This creates excessively negative pressure inside the thorax.

2. Flattened diaphragm & loss of zone of apposition

- The diaphragm is shortened and flattened from chronic hyperinflation.

- Instead of lifting the rib cage outward, contraction pulls inward on the lower ribs (Hoover's sign).

3. Weak or fatigued intercostal muscles

- Chronic overuse and poor mechanical advantage reduce their ability to stabilize the rib cage.

4. Increased chest wall compliance

- Especially in severe COPD, the chest wall can deform more easily under negative pressure.

Explain paradoxical breathing with COPD

During inspiration, the abdomen moves inward instead of outward (abdominal paradox). - The lower rib cage may move inward rather than expanding.

Why it occurs in COPD

- Chronic hyperinflation flattens and shortens the diaphragm.

- The diaphragm loses its normal dome shape and zone of apposition.

- When it contracts, it pulls the lower ribs inward rather than expanding them.

- High inspiratory effort exaggerates negative intrathoracic pressure, worsening the paradox.

Clinical significance

- Indicates advanced disease or respiratory muscle fatigue.

- Associated with increased work of breathing and dyspnea.

Vascular changes in COPD

- thickening of vessel wall and endothelial dysfunction

- increased vascular smooth muscle and infiltration of the vessel wall by inflammatory cells

- collagen deposition and emphysematous destruction of capillary bed (advanced stages)

- Structural changes lead to pulmonary hypertenion and right ventricular dysfunction

Two causes for VQ mismatch in COPD

both decrease ventilation;

- mucus plugging inflammation

- airway narrowing

Implications of hypoxemia in COPD

- Pulmonary vasoconstriction → ↑ pulmonary arterial pressure → pulmonary hypertension

- Right heart strain → cor pulmonale (right-sided heart failure)

- Secondary polycythemia → ↑ blood viscosity → ↑ thrombotic risk

- Reduced exercise tolerance → early fatigue and dyspnea

- Cognitive impairment → poor concentration, confusion (especially with exertion or sleep)

- Sleep disturbances → nocturnal desaturation

- Increased mortality and exacerbation risk

How does COPD lead to hypercapnia

Obstructive, inability to breath off CO2

Implications of hypercapnia in COPD

- Respiratory acidosis → renal bicarbonate retention (chronic compensation)

- Increased work of breathing and respiratory muscle fatigue

- Blunted ventilatory drive (chronic CO₂ retention)

- Morning headaches and daytime somnolence

- CO₂ narcosis (confusion, drowsiness, ↓ level of consciousness) in severe cases

- Increased risk of acute-on-chronic respiratory failure

- Worse prognosis and higher mortality

How is COPD a viscious downward spiral

Systemic inflammation -> muscle wasting and low physical activity capacity -> Low PA worsens COPD prognosis

What is finger clubbing and why do we see it in COPD patients

- Clubbing = painless widening and rounding of the fingertips and nails.

- In COPD, it is uncommon, usually associated with chronic hypoxia or coexisting conditions (e.g., bronchiectasis, lung cancer, or pulmonary fibrosis).

- Mechanism (theory): chronic hypoxia → vasodilation, increased blood flow, and connective tissue proliferation in the nail bed.

What are the three COPD severity rating systems

- MRC (medical research council) Dyspnea Scale

- GOLD (Global Initiative for COPD)

- CAT (COPD Assessment Test/CAAT (Chronic Airways Assessment Test)

What COPD Severity scale is used in Canada

mMRC Dyspnea Scale

What is the max. score on the COPD Assessment Test (CAT)

40 (MCID >2 points)

What are the goals for COPD management

- Prevent disease progression

- alleviate dyspnea and other symptoms

- improve exercise tolerance and daily activity

- treat AECOPD and complications (Acute Exacerbation COPD)

- improve health status

- improve QoL

- Reduce mortality

What is dyspnea

- subjective experience of breathing discomfort

- qualitatively distinct sensations; work effort, tightness, air hunger/unsatisfied inspiration

- distinct mechanisms and afferent pathwats for different sensations

- vary in intensity/unpleasantness

Explain the Dysnpnea cascade

1. respiratory center (brain stem) informed by;

- Central chemoreceptors (PO2) and Peripehral Chemoreceptors (PCO2)

- Sensory input (carotid & aortic bodies, stretch receptors, irritant receptors, C fibers, spindles & GTO)

- Cortical center

2. Repiratory center;

- sends motor plan to effectors via efferent pathways modulating respiratory muscle engagement

- communicates with the cortex to allow conscious control, perception, and interpretation of breathing

3. Cortical center is influenced by information from the respiratory center and psychological modifications

What is mismatch theory as it relates to dyspnea

Mismatch theory of dyspnea explains breathlessness as a discrepancy between the brain's drive to breathe and the feedback it receives.

Brief explanation:

- The brain increases respiratory motor drive (efferent signal)

- Sensory feedback from lungs, chest wall, and chemoreceptors (afferent signal) indicates that ventilation is inadequate or difficult

- This mismatch is perceived consciously as dyspnea

Example:

In COPD or restrictive lung disease, the brain commands stronger breathing, but airflow or lung expansion is limited → strong effort with poor result → breathlessness.

In short: 👉 Dyspnea occurs when "what the brain asks for" doesn't match "what the lungs deliver."

What four factors lead to hyperinflation in obstructive lung disease (in causal order)

1. Increased lung compliance:

Loss of elastic fibers → lungs are too easy to stretch, poor recoil

2. ↓ Airway tethering:

Reduced elastic recoil means less radial traction holding small airways open

3. ↓ Expiratory flow:

Airways narrow/collapse more easily during expiration (equal pressure point lower in airways)

4. Premature airway closure:

Small airways close before expiration is complete, trapping air

Leads to → Hyperinflation:

Trapped air accumulates → ↑ end-expiratory lung volume

How does hyperinflation lead to the etiology of dyspnea

1. stiff lungs → increased force generation required from diaphragm

2. Decreased ZoA → Decreased force generating capacity of diaphragm

3. decreased IRV → limited increases in VT

How does obstructive lung disease affect volumes in exercise

Higher ERV and lower IRV, decreased TV compared to healthy lung.

compare static and dynamic hyperinflation

Static:

- chronically increased lung volume at rest

- due to loss of elastic recoil and airway collapse

- ^ TLC, ^ FRC, ^ RV

Dynamic

- acute increase in lung volumes during activity or rapid breathing

- develops during exercise, tachypnea, or exacerbations

- ^ End-expiratory lung volume (EELV)

- exertional dyspnea

How does RR change with COPD in exercise compared to unaffected lungs

Sharp increase because tidal volume cannot increase to fill oxygen deficit

How is dyspnea quanitified? What are the limitations? Are there advantages of one over another?

The modified Borg Dyspnea Scale (0-10) or VAS (100 mm line)

Can only assess dyspnea at a single point in time, and should not be used retrospectively.

Borg is adventageous because;

- it has anchors/descriptors

- used to monitor exercise intensity

Why is ventilation limited in COPD

Ventilation can only be increased by increasing RR since VT change is limited. Therefore RR caps ventilation.

What questionnaires can be used to assess dyspnea? What are the benefits? What are the limitations?

- MRC (Medical research council)

- Chronic Respiratory Disease Questionnaire (CRQ)

- Baseline/Transitional Dyspnea Index (BDI/TDI)

- Pulmonary Fucntional Status and Dyspnea Questionnaire (PFSDQ)

- University of California at San Diego SOB Questionnaire (UCS-SOB Q)

Multidimensional approach; reliant on recall

What is the mMRC Dyspnea Scale

graded scale (0-4)

0 - Breathless with strenuous exercise

1 - shorf breath when hurrying on the level or walking up a slight hill (mild)

2 - walks slower than people of the same age on the level or stops for breath while walking at own pace on level (moderate)

3 - Stops for breath after walking 100 meters or after a few minutes on the level (moderate)

4 - Too breathless to leave the house or breathless when dressing (severe)

What does the Chronis Respiratory Disease Questionnaire consider/assess

- QoL

- 4 Domans (dyspnea, fatigue, emotional funcion, mastery)

- 7-point likert scale (higher score = better QoL)

- MCID - 0.5 points on a 7 point scale

6 Interventions for episodic dyspnea

- cognitive/psychological strategies

- breahting techniques & positioning

- air & O2

- drugs and medical devices

- environmental

- reduction og physical exertion

4 avenues for dyspnea treatment (4 Cs)

- reduce ventilatory demand (calm)

- reduce ventilatory obstruction (clear)

- improve respiratory muscle function (contract)

- alter the central perception of dypnea (CNS)

How can vetilatory demand be decreased to treat dyspnea

1. exercise training

- decreased lactate production

- improved mechanical efficiency of activity

- desensitization to dyspnea

2. energy convservation/ activity modification

3. decrease central drive

- supplemental O2 when hypoxemic

- pharmacotherapy in end stage (opiates, antidepresants, antianxiety)

- alter pulmonary afferent input (vibrations, fans, cool air)

How can vetilatory impedence be decreased to treat dyspnea

1. decrease airway narrowing

- pharmacotherapy (bronchodilators, anti inflammatory)

2. decrease hyperinflation

- pursed lip breathing

- lung volume reduction surgery

- endobronchial valves

- pharmacotherapy

What is the benefit of rollators for pt with COPD

- improved 6MWT distance

- lower end 6MWT borg dyspnea

- no effects on long term exercise capacity or health related quality of life (HRQOL)

What is the effect of inspiratory muscle training (IMT) on dyspnea due to COPD

IMT may not improve dyspnea, functional exercise capacity and QoL when assisted with PR (pulmonary rehabilitation)

- IMT is likely to improve these outcomes when provided alone

IMT strengthens breathing muscles, but when patients already do pulmonary rehab, it often doesn't translate into extra improvements in dyspnea, exercise tolerance, or quality of life.

How can central perception of dyspnea be altered?

- desensitization

- guided mastery

- relaxation

- yoga

- education (coping strategies, goal setting)