Week 7 Content.

Respiratory Investigations and Intro to Chest X-Rays

Respiratory Assessment- ABG Analysis

Arterial Blood Gas (first-line test): Evaluates gas exchange, lung +kidney function, acid-base status

Respiratory Assessment- Chest X-Ray

Diagnose lung/cardiac pathology, monitor progression

Tidal Volume (TV)

Volume of air in one breath (~500mL)

Minute Ventilation (MV)

MV = Respiratory Rate × TV (~6L/min)

Alveolar Ventilation (AV)

Air reaching alveoli (~4.2L/min)

Dead Space

inhaled air that does not participate in gas exchange -30% of air remains in conducting airways

Inspiratory Reserve Volume (IVR)

Volume of air able to inhaled over and above TV

Expiratory Reserve Volume (ERV)

Volume of air able to be forcefully exhaled after completion of respiratory cycle

Residual Volume (RV)

Volume of air remaining in lungs after maximum exhalation

Minimal Volume (MV)

Amount of air that would remain in your lungs if they were allowed to collapse

Inspiratory Capacity (IC)

Amount of air capable of being inhaled into lungs after completed respiratory cycle (TV+IRV)

Vital Capacity (VC)

Maximum amount of air that you can move into or out of your lungs in a single respiratory cycle (ERV+TV+IRV)

Functional Residual Capacity (FRC)

Amount of air remaining in your lungs after completing a respiratory cycle (ERV+RV)

Total Lung Capacity (TLC)

Total volume of your lungs (VC+RV)

Steps in Respiration (Gas Exchange)

1. Pulmonary Ventilation

2. External (Pulmonary) Respiration

3. Internal (Tissue) Respiration

Pulmonary Respiration

Consists of inhalation/exhalation

External Respiration

Gas exchange between alveoli and blood

Internal Respiration

Gas exchange between blood and tissue

Factors affecting Ventilation

1. Surface tension (Causes alveolar recoil, surfactant reduces surface tension= Respiratory Distress Syndrome)

2. Lung Compliance (High compliance = easy expansion, Low compliance = stiff lungs)

3. Diseases reducing compliance (TB, Pulmonary Oedema, ↓ Surfactant, Intercostal paralysis, Emphysema)

4. Airway resistance (bronchoconstriction ↑ resistance, bronchodilation ↓ resistance, (Asthma, COPD, Emphysema, CB))

V/Q Ratio (normally 0.8)

• ratio of the amount of air reaching the alveoli per minute (V) to the amount of blood reaching the alveoli per minute (Q)

• assesses the efficiency and adequacy of ventilation and perfusion

• (normally 0.8)

• Higher V/Q at Apex of Lungs- due to position relative to heart

• Lower V/Q at Base of Lungs- due to positon relative to heart

↑ V/Q Ratio

• ↑ ventilation or ↓ perfusion

• ↑ O₂

• ↓ CO₂

• Common in Pulmonary embolism and Emphysema

↓ V/Q Ratio

• ↓ ventilation or ↑ perfusion

• ↓ O₂

• ↑ CO₂

• Common in Asthma, Chronic bronchitis, Pulmonary oedema

Dalton’s Law

Total pressure= sum of partial pressures

Atmospheric Pressure (760mmHg) Equation

=PN2 + PO2 + PH2O + PCO2 + Pother gases

• PN2 = 597.4 mmHg

• PO2 = 158.8 mmHg

• PH2O = 3.0 mmHg

• PCO2 = 0.3 mmHg

• Pother gases = 0.5 mmHg

Factors Affecting Diffusion

• Partial pressure gradient

• Surface Area

• Solubility

• Diffusion Distance

Henry’s Law

• Quantity of a gas that will dissolve in a liquid is proportional to the partial pressures of the gas and its solubility

• Higher PP+Solubility= more gas staying in solution

Relationship between movement of O2 and CO2

• O₂ = Alveoli → blood → tissues

• CO₂ = Tissues → blood → alveoli

DLCO (Diffusion Capacity of Carbon Monoxide)

• Measures gas transfer efficiency using carbon monoxide (Normal ≥80%)

• Estimates transfer of oxygen from alveoli in your lungs to bloodstream

Factors ↑ DLCO

• Polycythaemia

• Asthma

• ↑ pulmonary blood volume

• Alveolar hemorrhage

Factors ↓ DLCO

Any conditon affecting effective alveolar surface area:

• Decrease of total lung area, e.g. restrictive lung disease

  -Chronic obstructive pulmonary disease (COPD) - except asthma

  -Pulmonary embolism

  -Cardiac insufficiency

  -Pulmonary hypertension

  -Chronic heart failure

Oxygen Transport

• 98.5% bound to haemoglobin

• Forms oxyhaemoglobin

• Hb saturation depends on PO₂

Oxyhaemoglobin Dissociation Curve

• Demonstrates how easily Haemoglobin picks up and lets go of oxygen.

• X-axis= PaO2- more oxygen avaliable as you move right

• Y-axis= % saturation of haemoglobin (How “full” haemoglobin is with oxygen)

ODC- Left Shift

The curve moves LEFT when Hb has a higher affinity for oxygen (Hb grabs oxygen easily, does NOT want to let it go to tissues)

Caused by lower CO₂, Higher pH (less acidic), Lower temperature

Happens when body is more “resting” or calm

haemoglobin is MORE saturated → helps oxygen loading

ODC- Right Shift

The curve moves RIGHT when Hb has a lower affinity for oxygen (Hb lets oxygen go more easily)

Caused by Higher CO₂, Lower pH (more acidic), Higher temperature

happens in active tissues like exercising muscle, fever, metabolically active tissue

These tissues need more oxygen → haemoglobin unloads oxygen there.

CARBON DIOXIDE TRANSPORT

• 7% dissolved in plasma

• 23% bound to Hb

• 70% as bicarbonate (HCO₃⁻)

Normal Acid-Base Balance

Normal pH = 7.35-7.45

Acidosis (acidaemia if refering to blood)

pH <7.35 (too acidic). Caused by increased CO2 → increased hydrogen ion concentration→ lowers pH

Alkalosis (alkalaemia if refering to blood)

pH >7.45 (Not acidic enough). Caused by reducing CO2 → decreases level of carbonic acid→raises pH

Blood Buffer Systems

• Prevent rapid changes in pH by rapidly binding H+ ions

• Made of weak acid and weak base

• 2 important systems: protein and cardonic acid-bicarbonage buffer systems

Protein Buffer System

Intracellular fluid and blood plasma

 Albumin in blood plasma→ Functional groups of amino acids: Amines (base) and Carboxyl group (acid)

 Hb within RBCs→ Buffers H+→Deoxyhemoglobin collects H+ to reduce acidity of RBCs

Carbonic Acid-Bicarbonate Buffer System

Bicarbonate ion- weak base

Carbonic acid- weak acid

Does not function when there is a shortage of CO2

Respiratory Regulation

• ↑ CO₂ or H+ →stimulates respiratory→increased ventilation→ exhales CO2→elimates excess acid

• Hyperventilation ↓ CO₂

• Hypoventilation ↑ CO₂

• Fast response

Renal Regulation

Abnormal pH→kidneys conserve/eliminate H+ and carbonic acid

• If acidotic = eliminates H+ and retains carbonc acid

• If alkalotic = elimiates carbonic acid

• Slow response

Central Chemoreceptors

• In ventral sruface of medulla

• Detect CO₂ via changes in pH

Peripheral Chemoreceptors

• in carotid and aortic bodies

• respond to changes in O₂, and CO₂ and pH

Ventilation Response to Carbon dioxide

• CO₂ = main breathing stimulus- increases TV and Respiratory rate

• Dueing exercise, CO2 production is increased but little to no change in PaCO2

• PaCO2 set point buffered during COPD

Ventilatory response to oxygen

• arterial blood oxygen tension (PaO 2) less tightly regulated

• respiratory stimulation dictated by PaCO 2 prevents critical

falls in oxygenation

• signalling from carotid bodies increases as PaO 2 falls

• firing rates increase within seconds in range of 60 – 80

mmHg

• inflexion point for hypoxic ventilatory responsiveness

• coincides with beginning of steep portion of oxyhaemaglobin

dissociation curve

Acid Base disorders- Respiratory Acidosis

↑ PaCO₂ from hypoventilation

Low pH

-lungs (primary mechanism by which [H+] is adjusted)

Acid Base disorders- Respiratory Alkalosis

↓ CO₂ from hyperventilation

High pH

-lungs (primary mechanism by which [H+] is adjusted)

Acid Base disorders- Metabolic Acidosis

↓ bicarbonate or ↑ acid

Acid Base disorders- Metabolic Alkalosis

↑ bicarbonate

Respiratory Acidosis- Pathophysiology

• Inadequate alveolar ventilation (CNS depression (stroke), medication depression, neuromuscular disorders, lung/chest infections, airway obstruction)

• Overproduction of CO2 (hypercatabolic states e.g. sepsis)

• Increased intake (Rebreathing CO2 containing gases, Insufflation of CO2 into body)

Respiratory Alkalosis- Pathophysiology

• increased expiration and pH increases as less carbonic acid created

• Causes: Central (head injury), hyperventilation (pain, panic), medication, pulmonary due to hypoxaemia (PE, altitude)

Ventilatory response to hydrogen ions

• Increased H⁺ stimulates carotid bodies→Ventilation increases to reduce PaCO₂

• Lower PaCO₂ raises pH and decreases central chemoreceptor stimulation.

• This partly offsets increased ventilation and helps compensate for metabolic acidosis.

• pH regulation has priority over PaCO₂ homeostasis.

Metabolic acidosis- Pathophysiology

Increases concentration of [H+] and reduces bicarbonate concentration. Caused by:

• lactic acidosis, ketoacidosis

• diarrhoea

• reduced renal acid excretion

Metabolic alkalosis- Pathophysiology

Loss of hydrogen ions, produces elevation of bicarbonate and pH. Caused by:

• vomiting

• hypovolemia

• diuretic use

• administration bicarbonate

Compensation

METABOLIC problem= Carbonic acid abnormality→ LUNGS change PaCO2

RESPIRATORY problem= PaCO2 abnormality→ KIDNEYS cahnge carbonic acid

(more HCO3= more alkaline, more CO2= more acidic)

Hypoxaemia- Pathophysiology

• Defiency of oxygen in arterial blood

• PaO2 <60mmHg

• SaO2 <90%

Hypoxia- Pathophysiology

• Reduced oxygen to the body or at specific tissues

6 Steps in ABG analysis and Interpretation

1. the pH normal? (7.35-7.45)- Normal (compensated acidemia if below 7.35)

2. the PaCO2 normal? (35-45mmHg)

3. the HCO3 normal? (22-26 mEq/L)

4. Match the CO2 or the HCO3 with the pH

5. Does the CO2 or the HCO3 go the opposite direction of the pH?

6. Are the pO2 and the O2 saturation normal?