Lexa Comprehensive Respiratory Physiology and Nursing Care Review

Q: What are the four components of respiratory clinical judgment?

Noticing, interpreting, responding, and reflecting.

Q: What does the noticing phase of respiratory clinical judgment involve?

Recognizing abnormal cues such as risk factors, assessment findings, and changes in respiratory status.

Q: What does the interpreting phase of respiratory clinical judgment involve?

Analyzing cues to determine whether the problem involves ventilation, diffusion, or perfusion.

Q: What does the responding phase of respiratory clinical judgment involve?

Implementing appropriate nursing interventions based on the identified problem.

Q: What does the reflecting phase of respiratory clinical judgment involve?

Evaluating the patient's response to interventions and modifying care as needed.

Q: What are modifiable risk factors for respiratory disease?

Smoking, exposure to chemicals or particulates, inactivity, and obesity.

Q: What are non-modifiable risk factors for respiratory disease?

Family history or genetics, asthma, exposure history, and alpha-1 antitrypsin deficiency.

Q: What is the most significant modifiable risk factor for respiratory disease?

Smoking.

Q: What is ventilation in respiratory physiology?

The mechanical transfer of air between the lungs and the atmosphere to move oxygen in and carbon dioxide out.

Q: What is the primary goal of ventilation?

To bring oxygen into the lungs and remove carbon dioxide from the body.

Q: What is diffusion in respiratory physiology?

The passive exchange of oxygen and carbon dioxide across the alveolar-capillary membrane.

Q: Where does diffusion primarily occur in the respiratory system?

At the alveolar and capillary level.

Q: What is perfusion in respiratory physiology?

The circulation and delivery of oxygen-rich blood throughout the body for tissue-level gas exchange.

Ventilation, Diffusion, and Perfusion Impairments

Q: What types of ventilation impairments can occur in respiratory disease?

Obstructive, restrictive, or mixed impairments.

Q: What causes diffusion impairments in the lungs?

Thickened membranes, obstruction, or reduced driving pressures.

Q: What causes perfusion impairments in the respiratory system?

Pump failure, vascular dysfunction, or reduced oxygen-carrying capacity.

Q: What does the ventilation-perfusion ratio describe?

The balance between alveolar ventilation and pulmonary perfusion.

Q: What is the normal V/Q ratio?

Approximately 0.8-1.

Q: Why is V/Q matching important?

Optimal gas exchange requires ventilation and perfusion to be balanced.

Q: Why are not all alveoli ventilated at all times?

Ventilation varies depending on lung regions and physiologic conditions.

Q: Why is oxygen considered a pulmonary vasodilator?

Oxygen reduces pulmonary vasoconstriction and increases blood flow to ventilated alveoli.

Q: What defines a low V/Q state?

Perfusion exceeds ventilation, resulting in poor gas exchange.

Q: What are common causes of low V/Q (functional shunt)?

Atelectasis, pulmonary edema, and asthma.

Q: What defines a high V/Q state?

Ventilation exceeds perfusion, resulting in inadequate gas exchange.

Q: What are common causes of high V/Q (dead space)?

Pulmonary embolism and cardiogenic shock.

Q: What primarily stimulates breathing in healthy individuals?

Changes in carbon dioxide detected by central chemoreceptors.

Q: How sensitive are central chemoreceptors to CO₂ changes?

They respond to small changes of 1-2 mmHg in PaCO₂.

Q: When do peripheral chemoreceptors significantly stimulate breathing?

When PaO₂ drops below 60 mmHg.

Q: What is the hypoxic drive theory in COPD?

The theory that chronically elevated CO₂ leads to reliance on low oxygen levels to stimulate breathing.

Q: Why is hypoxic drive theory considered oversimplified?

Because ventilation-perfusion mismatch is the main cause of CO₂ retention, not loss of respiratory drive.

Q: Why can high oxygen administration increase PaCO₂ in COPD patients?

Oxygen worsens ventilation-perfusion mismatch and reduces pulmonary vasoconstriction.

Q: What is the primary reason PaCO₂ rises in COPD patients receiving oxygen?

Ventilation-perfusion mismatch.

Q: What is the Haldane effect?

Oxygenated hemoglobin carries less carbon dioxide, increasing CO₂ levels in the blood.

Q: How much does the Haldane effect contribute to CO₂ retention?

Approximately 25%.

Q: What oxygen saturation range is typically targeted in COPD patients?

88%-92%.

Q: Why is oxygen considered a "Q" intervention rather than a "V" intervention?

Oxygen improves perfusion and oxygenation but does not correct ventilation problems.

Q: What nursing interventions improve ventilation?

Elevating the head of the bed and administering bronchodilators.

Q: Why is reassessment essential after oxygen administration?

To evaluate effectiveness and prevent worsening CO₂ retention.

Q: What characterizes obstructive pulmonary disease?

Difficulty getting air out of the lungs due to air trapping.

Q: What are common obstructive pulmonary diseases?

Asthma, COPD, cystic fibrosis, bronchiectasis, and acute bronchitis.

Q: What characterizes restrictive pulmonary disease?

Difficulty getting air into the lungs due to reduced lung volume and expansion.

Q: What are parenchymal causes of restrictive lung disease?

Fibrosis, pneumonia, and asbestosis.

Q: What are external causes of restrictive lung disease?

Obesity, pleural effusions, and ascites.

Q: What is hyperventilation and what does it result in? What happens to PaCO₂?

Hyperventilation is an increased rate or depth of breathing that exceeds metabolic needs, causing excessive CO₂ elimination, resulting in hypocapnia (PaCO₂ < 35 mm Hg) and respiratory alkalosis.

Q: What ABG pattern is seen with hyperventilation?

Respiratory alkalosis with decreased PaCO₂ (<35 mm Hg) and elevated pH (>7.45).

Q: What is hypoventilation and what does it result in?

Hypoventilation occurs when respirations are too slow or shallow to meet metabolic needs, leading to CO₂ retention and decreased oxygen levels.

Q: What causes hypoventilation?

Alterations in pulmonary mechanics or neurological control of breathing.

Q: What happens to PaCO₂ in hypoventilation?

PaCO₂ increases, causing hypercapnia (PaCO₂ > 44-45 mm Hg).

Q: What ABG pattern is seen with hypoventilation?

Respiratory acidosis with elevated PaCO₂ (>45 mm Hg) and decreased pH (<7.35).

Q: What is hypoxia?

Hypoxia is a decrease in oxygen supply to tissues and cells.

Q: Why does hypoxia lead to metabolic acidosis?

Inadequate oxygen delivery causes anaerobic metabolism and lactic acid production.

Q: What ABG pattern is associated with hypoxia?

Metabolic acidosis with decreased pH and decreased bicarbonate (HCO₃⁻).

Q: What is hypoxemia?

Hypoxemia is reduced oxygenation of arterial blood, indicated by decreased PaO₂.

Q: What causes hypoxemia related to hypoventilation?

Increased alveolar CO₂ reduces alveolar oxygen, resulting in less oxygen available for diffusion into the blood.

Q: How does V/Q mismatch cause hypoxemia?

Blood flows past poorly ventilated alveoli, leading to inadequate oxygenation of arterial blood.

Q: Which conditions commonly cause hypoxemia due to V/Q mismatch or shunting?

Atelectasis, asthma, pulmonary edema, pneumonia, and shunting.

Q: How does thickening of the alveolocapillary membrane cause hypoxemia?

Edema or fibrosis increases diffusion distance, impairing oxygen transfer.

Q: How does emphysema cause hypoxemia?

Destruction of alveoli reduces surface area for gas exchange.

Q: What ABG pattern may be seen with prolonged hypoxemia?

Metabolic acidosis due to tissue hypoxia and lactic acid production.

Q: What is hypercapnia?

Hypercapnia is an increase in CO₂ levels in arterial blood.

Q: What is the primary cause of hypercapnia?

Hypoventilation of the alveoli.

Q: What neurological conditions can cause hypercapnia?

Depression of the respiratory center from medications, CNS infections, brain trauma, or medullary disease.

Q: How do neuromuscular disorders contribute to hypercapnia?

They impair respiratory muscle function, reducing effective ventilation.

Q: How do thoracic cage abnormalities cause hypercapnia?

They limit chest expansion, leading to inadequate ventilation.

Q: Why does emphysema cause hypercapnia?

Increased physiological dead space and increased work of breathing impair CO₂ elimination.

Q: What ABG pattern is seen with hypercapnia?

Respiratory acidosis with elevated PaCO₂ and decreased pH.

Spirometry

is an instrument that can be used to measure PFTs such as tidal volume, minute ventilation, and vital capacity

measures how well your lungs work; extent of dysfunction

measures how much volume and how fast you can move air into and out of the lungs

performed by having the patient sit in a semi-fowler's position using diaphragmatic breathing, breathing slowly in (holding or 3 seconds) and exhaling

PE, cardiogenic shock → high V/Q (dead space)

→ high V/Q (dead space)

Atelectasis, pneumonia, asthma, pulmonary edema

→ low V/Q (shunt)

Emphysema

→ diffusion + dead space

Pulmonary edema/fibrosis

→ diffusion problem

High altitude

→ ↓ FiO₂

↓ FiO₂ (e.g. high altitude)

Hypoventilation

V/Q mismatch

Diffusion impairment

↓ Pulmonary perfusion

Hypoxemia trigger/mechanisms

q: What is restrictive lung disease?

Impaired inhalation due to limited lung expansion causing reduced lung volumes and impaired oxygenation.

q: What is the main problem in intrinsic restrictive lung disease?

Lung tissue itself becomes stiff and thick, impairing diffusion.

q: Give an example of intrinsic restrictive lung disease.

Pulmonary fibrosis.

q: What happens to alveoli in intrinsic restrictive disease?

They become thick, stiff, and lose elasticity, impairing gas diffusion.

q: What type of problem dominates intrinsic restrictive disease?

Diffusion problem.

q: What is the main problem in extrinsic restrictive lung disease?

Lungs are compressed and cannot expand despite normal lung tissue.

q: Give examples of extrinsic restrictive lung disease.

Pleural effusion, atelectasis, obesity, chest wall disorders.

q: How is restrictive lung disease generally treated?

Treat the underlying cause and support the patient's oxygenation and ventilation.

q: What supportive nursing interventions are used in restrictive lung disease?

Oxygen therapy, upright positioning, breathing exercises, energy conservation.

q: What is a shunt?

Blood passes through non-ventilated alveoli causing hypoxemia poorly responsive to oxygen.

q: What is atelectasis?

Airless collapse of alveoli reducing surface area for gas exchange.

q: What are common signs and symptoms of atelectasis?

SOB, hypoxia/hypoxemia.

q: What imaging is used to diagnose atelectasis?

Chest X-ray or CT scan.

q: What are common causes of atelectasis?

Post-surgical state, pain/splinting, mucus plug, obstruction, surfactant deficiency.

q: What type of dysfunction does atelectasis cause?

Ventilation and diffusion disturbance resulting in a shunt.

q: What are the three types of atelectasis?

Compressive, absorption, surfactant impairment.

q: What causes compressive atelectasis?

External pressure such as pleural effusion or pneumothorax.

q: What causes absorption atelectasis?

Removal of air due to obstruction or hypoventilation, commonly mucus plugs.

q: What causes surfactant-impairment atelectasis?

ARDS or mechanical ventilation.

q: What are key nursing interventions for atelectasis?

PEEP/CPAP/BiPAP, deep breathing and coughing, bronchoscopy.

q: What is the overall goal in treating atelectasis?

Re-expand collapsed alveoli and improve ventilation.

q: What is PEEP?

Pressure maintained at end expiration to prevent alveolar collapse.

q: What does CPAP provide?

Continuous pressure with PEEP only to improve oxygenation.

q: What does BiPAP provide?

Inspiratory pressure plus PEEP to support ventilation.

q: When is bronchoscopy used in atelectasis?

When a mucus plug is suspected.

q: What is pneumothorax?

Air escaping from the lung into the pleural space.