MED SURG / PATHO – EXAM II
UNIT 3
ALTERATIONS IN PULMONARY FUNCTION
HYPOventilation HYPERventilation
Air delivered to alveoli = Insufficient to provide oxygen (O2) + Increased amount of air entering the alveoli
Remove carbon dioxide (CO2) ● Decreased PaCO2 ( <35 mmHg) – Hypocapnia
● Increased PaCO2 (>45 mmHg) – Hypercapnia + ○ Low CO2 level
Hypoxemia ● Increased rate and depth of respiration
○ Increased alveolar CO2 displaces oxygen ● Respiratory Alkalosis
● Decreased rate and depth of respiration (Bradypnea)
● Drugs → Morphine + Barbiturates (Depress Central Most Common:
Respiratory Drive) ● Pain
● Obesity (Pickwickian Syndrome) ● Fever
● Myasthenia gravis (Muscle weakness) ● Anxiety
● Obstructive Sleep Apnea
● Chest wall damage Less Common:
● Paralysis of respiratory muscles (diaphragm) ● Obstructive + Restrictive lung diseases
● Pain r/t Sx of thorax/abdomen ● Sepsis
○ Hypoventilation secondary to decreased ● High altitude
inspiration ● Brainstem injury (Central Neurogenic Hyperventilation)
Physiologic Cause of Hyperventilation:
● Hypoxic stimulation of peripheral chemoreceptors
○ Decreased O2 → Peripheral chemoreceptors detect this + Send signals to INCREASE breathing rate → Delivering more
oxygen to the body
Hyperventilation = Normal response to High Altitude (Compensatory Mechanism to decrease PaCO2)
● ↓ Decreased Oxygen (O2) in the air → Body compensates by HYPERventilating (Breathing Faster + Deeper)
○ Hyperventilation → ↓ Decreased PaCO2 in the blood
■ ↓ Decreased PaCO2 in the blood → “Left-shift” on oxygen-hemoglobin curve
● Hemoglobin holds onto oxygen more tightly → Which helps with the ↓ Decreased O2 in the air
Ineffective Gas Exchange + Ventilatory Failure
● Gas exchange fails when:
1. Air is not distributed evenly within the lungs (Maldistribution)
2. Breathing volume / Minute ventilation = Decreased
3. Alveoli are not properly ventilated (Alveolar Hypoventilation)
● Maldistribution of gas (Uneven airflow) → Emphysema (Alveolar sacs don’t function well)
Obstructive Pulmonary Diseases
● Asthma, Chronic Bronchitis, & Emphysema → Increased airway RESISTANCE due to:
1. Obstruction of airways from increased sputum production (Mucus blocking airways)
2. Mucosal Hypertrophy + Edema (Thickening + Swelling of airway walls)
3. Loss of structural integrity of the airway
4. Narrowing of airway from bronchial smooth muscle contraction → Hyperactivity of airways (Tightening of airway
muscles; Bronchospasm)
● During Expiration → AIR LEAVES AREAS OF LEAST RESISTANCE FIRST → Maldistribution of gas
Hypoxemia Hypoxia
Deficient levels of BLOOD oxygen Decreased TISSUE oxygenation
● LOW ARTERIAL O2 CONCENTRATION ● Difficult to measure
● LOW HEMOGLOBIN SATURATION ● Blood flow + PaO2 = Low
● Decreased blood flow → Decreased oxygen delivery
Measured by: Arterial Blood Gas (ABG) + Pulse Oximetry - O2
Saturation
, Types of Hypoxia
Hypoxic Hypoxia DECREASED PaO2 + NORMAL O2-carrying capacity (Hgb)
(Low oxygen in the blood despite normal hemoglobin)
Etiology:
● High altitude (less oxygen in the air)
● Hypoventilation (breathing too shallow/slow)
● Airway obstruction (blockage of airflow)
Tx: Oxygen Therapy
Anemic Hypoxia DECREASED O2-carrying capacity (Hgb)
(Not enough hemoglobin to carry oxygen)
Etiology: Any disorder resulting in LOW HEMOGLOBIN CONCENTRATION
● Anemia
● Blood loss
Key Point: Even if oxygen is available, there is not enough “transport” (Hgb) to carry it
Circulatory Hypoxia LOW CARDIAC OUTPUT state
● NORMAL O2-carrying capacity (Hgb)
● REDUCED Blood flow
(Normal oxygen levels and hemoglobin, but reduced blood flow to tissues)
Etiology:
● Shock
● Cardiac arrest
● Severe blood loss
● Thyrotoxicosis
● Congestive heart failure (CHF)
Histotoxic Hypoxia DECREASED O2-carrying capacity (Hgb) due to a TOXIC SUBSTANCE
(Tissues cannot use the oxygen, even if it is delivered, because of toxic interference)
Etiology:
● Cyanide poisoning
Ineffective gas exchange occurs when:
● Ventilation + Perfusion = Mismatch
● Diffusion abnormalities exist
● Right-to-left shunt exists
Capillary Recruitment + Distention:
● Not ALL lung capillaries are open during normal conditions → The body does not need them all the time
● When more blood flow is needed (exercise) → the lungs:
○ Recruit: OPEN previously closed capillaries
○ Distend: EXPAND capillaries that are already open
● This increases blood flow to alveoli (air sacs) → Improve oxygen exchange when required
Deoxygenated Blood Mixing:
● 2% of the total blood flow in the lung is not oxygenated
1. Thebesian veins (drain blood from the heart walls)
2. Pleural veins (from the lung’s lining)
3. Bronchial veins (drain blood from airways)
● Drain deoxygenated blood → Left side of the heart → Pulmonary veins
, OBSTRUCTIVE PULMONARY DISORDERS
Acute Bronchitis
Etiology ● ACUTE inflammation of the trachea and bronchi
● Highest incidence: Smokers, Young children, & Elderly (Winter months)
● Viral
○ Influenza A/B, Parainfluenza virus, Respiratory Syncytial Virus (RSV), Coronavirus, Rhinovirus, Coxsackie
virus, & Adenovirus
● Nonviral
○ Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma, Moraxella, & Chlamydia pneumoniae
● Heat
● Inhalation of Smoke/Chemicals
○ Sulfur dioxide, Chlorine, Bromine, Fluorine gas
● Allergic reactions
Pathogenesis Airways become INFLAMED + NARROWED
● Capillary dilation
○ First response to infection/irritants → Blood vessels widen → Increase blood flow → Increase immune cells to
area → Fight infection
● Swelling from fluid exudation
○ Capillaries dilate → Fluid leaks into surrounding tissues → Swelling narrows airways → Harder to breathe
● Infiltration w/ inflammatory cells
○ Immune cells → Bronchial walls → Combat infection → Increases inflammation → Narrows airway
● Increased mucus production
○ Inflamed airways produce more mucus (protective response) → Excess mucus blocks airways →
Coughing/Dyspnea
● Loss of ciliary function
○ Cilia help clear mucus + become less effective with inflammation → Mucus = not cleared
● Loss of portions of ciliated epithelium
○ Prolonged inflammation → Damages epithelial lining of airways → Cilia = lost → Mucus = not cleared
Dx ● Distinct hallmark of disease → Recent onset of cough
● Chest radiograph (x-ray) → Distinguishes acute bronchitis from pneumonia
Clinical Manifestations ● Usually Mild + Self-limiting
● Cough (Productive/Nonproductive)
● Low-grade fever
● Substernal chest discomfort
● Sore throat
● Postnasal drip
● Fatigue
, OBSTRUCTIVE PULMONARY DISORDERS
Chronic Bronchitis
Etiology ● Cigarette Smoking (90%)
● Repeated airway infections
● Genetic predisposition
● Inhalation of physical/chemical irritants
● Chronic or Recurrent productive cough > 3 months > 2 consecutive years
● Type B COPD → “Blue bloater”
● Hypersecretion of bronchial mucus
● Persistent + Irreversible w/ Emphysema
Risk Factors:
● Overweight man/woman // (1:2 male-to-female ratio) // ≥ 30-40 years // Hx of smoking
Pathogenesis ● Chronic Inflammation + Swelling → Bronchial Mucosa → Scarring (Fibrosis of mucous membrane)
○ Extends → Surrounding alveoli // Narrowed airway + Mucous plugs prevent proper oxygenation → Airway
obstruction
● Hyperplasia → Bronchial mucosal glands + Goblet cells (decreased ciliary function)
○ Increased mucus production + Formation of mucus plugs
● Increased Bronchial Wall Thickness
○ AIRFLOW RESISTANCE increases work of breathing → INCREASED oxygen (O2) demands
○ Ventilation-Perfusion mismatch → Hypoxemia + Hypercarbia → Increases pulmonary artery resistance
● Pulmonary Hypertension
○ Inflammation in bronchial walls + vasoconstriction of pulmonary vessels + arteries
○ Right-sided heart failure may occur r/t pulmonary resistance
● Destruction of Bronchial Walls
○ Dilation of airway sacs (Bronchiectasis)
Inflammation → Neutrophil activity→ Interleukin-8 levels ↑ // CD8 T-lymphocyte levels ↑ // Eosinophils ↑
Dx ● Chest x-ray
○ ↑ Bronchial vascular markings, Congested lung fields, Enlarged horizontal cardiac silhouette, Evidence of
previous infection
● Pulmonary function tests
○ Normal total lung capacity (TLC), ↑ Residual volume (RV), ↓ FEV
● Arterial blood gas (ABG)
○ ↑ PaCO2 (Carbon dioxide) + ↓ PaO2 (Oxygen) (< 65 mmHg)
● ECG
○ Atrial dysrhythmias + Right ventricular hypertrophy
● Physical Examination
○ Scattered crackles, Rhonchi, Wheezes; Use of accessory muscles; Jugular vein distention; Clubbing;
Pedal/Ankle edema
Clinical Manifestations ● Overweight
● Commonly associated with emphysema
● Exertional dyspnea
● Excessive sputum
● Chronic cough (more severe in morning)
● Excess body fluids (edema, hypervolemia)
● Cyanosis (LATE SIGN)
UNIT 3
ALTERATIONS IN PULMONARY FUNCTION
HYPOventilation HYPERventilation
Air delivered to alveoli = Insufficient to provide oxygen (O2) + Increased amount of air entering the alveoli
Remove carbon dioxide (CO2) ● Decreased PaCO2 ( <35 mmHg) – Hypocapnia
● Increased PaCO2 (>45 mmHg) – Hypercapnia + ○ Low CO2 level
Hypoxemia ● Increased rate and depth of respiration
○ Increased alveolar CO2 displaces oxygen ● Respiratory Alkalosis
● Decreased rate and depth of respiration (Bradypnea)
● Drugs → Morphine + Barbiturates (Depress Central Most Common:
Respiratory Drive) ● Pain
● Obesity (Pickwickian Syndrome) ● Fever
● Myasthenia gravis (Muscle weakness) ● Anxiety
● Obstructive Sleep Apnea
● Chest wall damage Less Common:
● Paralysis of respiratory muscles (diaphragm) ● Obstructive + Restrictive lung diseases
● Pain r/t Sx of thorax/abdomen ● Sepsis
○ Hypoventilation secondary to decreased ● High altitude
inspiration ● Brainstem injury (Central Neurogenic Hyperventilation)
Physiologic Cause of Hyperventilation:
● Hypoxic stimulation of peripheral chemoreceptors
○ Decreased O2 → Peripheral chemoreceptors detect this + Send signals to INCREASE breathing rate → Delivering more
oxygen to the body
Hyperventilation = Normal response to High Altitude (Compensatory Mechanism to decrease PaCO2)
● ↓ Decreased Oxygen (O2) in the air → Body compensates by HYPERventilating (Breathing Faster + Deeper)
○ Hyperventilation → ↓ Decreased PaCO2 in the blood
■ ↓ Decreased PaCO2 in the blood → “Left-shift” on oxygen-hemoglobin curve
● Hemoglobin holds onto oxygen more tightly → Which helps with the ↓ Decreased O2 in the air
Ineffective Gas Exchange + Ventilatory Failure
● Gas exchange fails when:
1. Air is not distributed evenly within the lungs (Maldistribution)
2. Breathing volume / Minute ventilation = Decreased
3. Alveoli are not properly ventilated (Alveolar Hypoventilation)
● Maldistribution of gas (Uneven airflow) → Emphysema (Alveolar sacs don’t function well)
Obstructive Pulmonary Diseases
● Asthma, Chronic Bronchitis, & Emphysema → Increased airway RESISTANCE due to:
1. Obstruction of airways from increased sputum production (Mucus blocking airways)
2. Mucosal Hypertrophy + Edema (Thickening + Swelling of airway walls)
3. Loss of structural integrity of the airway
4. Narrowing of airway from bronchial smooth muscle contraction → Hyperactivity of airways (Tightening of airway
muscles; Bronchospasm)
● During Expiration → AIR LEAVES AREAS OF LEAST RESISTANCE FIRST → Maldistribution of gas
Hypoxemia Hypoxia
Deficient levels of BLOOD oxygen Decreased TISSUE oxygenation
● LOW ARTERIAL O2 CONCENTRATION ● Difficult to measure
● LOW HEMOGLOBIN SATURATION ● Blood flow + PaO2 = Low
● Decreased blood flow → Decreased oxygen delivery
Measured by: Arterial Blood Gas (ABG) + Pulse Oximetry - O2
Saturation
, Types of Hypoxia
Hypoxic Hypoxia DECREASED PaO2 + NORMAL O2-carrying capacity (Hgb)
(Low oxygen in the blood despite normal hemoglobin)
Etiology:
● High altitude (less oxygen in the air)
● Hypoventilation (breathing too shallow/slow)
● Airway obstruction (blockage of airflow)
Tx: Oxygen Therapy
Anemic Hypoxia DECREASED O2-carrying capacity (Hgb)
(Not enough hemoglobin to carry oxygen)
Etiology: Any disorder resulting in LOW HEMOGLOBIN CONCENTRATION
● Anemia
● Blood loss
Key Point: Even if oxygen is available, there is not enough “transport” (Hgb) to carry it
Circulatory Hypoxia LOW CARDIAC OUTPUT state
● NORMAL O2-carrying capacity (Hgb)
● REDUCED Blood flow
(Normal oxygen levels and hemoglobin, but reduced blood flow to tissues)
Etiology:
● Shock
● Cardiac arrest
● Severe blood loss
● Thyrotoxicosis
● Congestive heart failure (CHF)
Histotoxic Hypoxia DECREASED O2-carrying capacity (Hgb) due to a TOXIC SUBSTANCE
(Tissues cannot use the oxygen, even if it is delivered, because of toxic interference)
Etiology:
● Cyanide poisoning
Ineffective gas exchange occurs when:
● Ventilation + Perfusion = Mismatch
● Diffusion abnormalities exist
● Right-to-left shunt exists
Capillary Recruitment + Distention:
● Not ALL lung capillaries are open during normal conditions → The body does not need them all the time
● When more blood flow is needed (exercise) → the lungs:
○ Recruit: OPEN previously closed capillaries
○ Distend: EXPAND capillaries that are already open
● This increases blood flow to alveoli (air sacs) → Improve oxygen exchange when required
Deoxygenated Blood Mixing:
● 2% of the total blood flow in the lung is not oxygenated
1. Thebesian veins (drain blood from the heart walls)
2. Pleural veins (from the lung’s lining)
3. Bronchial veins (drain blood from airways)
● Drain deoxygenated blood → Left side of the heart → Pulmonary veins
, OBSTRUCTIVE PULMONARY DISORDERS
Acute Bronchitis
Etiology ● ACUTE inflammation of the trachea and bronchi
● Highest incidence: Smokers, Young children, & Elderly (Winter months)
● Viral
○ Influenza A/B, Parainfluenza virus, Respiratory Syncytial Virus (RSV), Coronavirus, Rhinovirus, Coxsackie
virus, & Adenovirus
● Nonviral
○ Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma, Moraxella, & Chlamydia pneumoniae
● Heat
● Inhalation of Smoke/Chemicals
○ Sulfur dioxide, Chlorine, Bromine, Fluorine gas
● Allergic reactions
Pathogenesis Airways become INFLAMED + NARROWED
● Capillary dilation
○ First response to infection/irritants → Blood vessels widen → Increase blood flow → Increase immune cells to
area → Fight infection
● Swelling from fluid exudation
○ Capillaries dilate → Fluid leaks into surrounding tissues → Swelling narrows airways → Harder to breathe
● Infiltration w/ inflammatory cells
○ Immune cells → Bronchial walls → Combat infection → Increases inflammation → Narrows airway
● Increased mucus production
○ Inflamed airways produce more mucus (protective response) → Excess mucus blocks airways →
Coughing/Dyspnea
● Loss of ciliary function
○ Cilia help clear mucus + become less effective with inflammation → Mucus = not cleared
● Loss of portions of ciliated epithelium
○ Prolonged inflammation → Damages epithelial lining of airways → Cilia = lost → Mucus = not cleared
Dx ● Distinct hallmark of disease → Recent onset of cough
● Chest radiograph (x-ray) → Distinguishes acute bronchitis from pneumonia
Clinical Manifestations ● Usually Mild + Self-limiting
● Cough (Productive/Nonproductive)
● Low-grade fever
● Substernal chest discomfort
● Sore throat
● Postnasal drip
● Fatigue
, OBSTRUCTIVE PULMONARY DISORDERS
Chronic Bronchitis
Etiology ● Cigarette Smoking (90%)
● Repeated airway infections
● Genetic predisposition
● Inhalation of physical/chemical irritants
● Chronic or Recurrent productive cough > 3 months > 2 consecutive years
● Type B COPD → “Blue bloater”
● Hypersecretion of bronchial mucus
● Persistent + Irreversible w/ Emphysema
Risk Factors:
● Overweight man/woman // (1:2 male-to-female ratio) // ≥ 30-40 years // Hx of smoking
Pathogenesis ● Chronic Inflammation + Swelling → Bronchial Mucosa → Scarring (Fibrosis of mucous membrane)
○ Extends → Surrounding alveoli // Narrowed airway + Mucous plugs prevent proper oxygenation → Airway
obstruction
● Hyperplasia → Bronchial mucosal glands + Goblet cells (decreased ciliary function)
○ Increased mucus production + Formation of mucus plugs
● Increased Bronchial Wall Thickness
○ AIRFLOW RESISTANCE increases work of breathing → INCREASED oxygen (O2) demands
○ Ventilation-Perfusion mismatch → Hypoxemia + Hypercarbia → Increases pulmonary artery resistance
● Pulmonary Hypertension
○ Inflammation in bronchial walls + vasoconstriction of pulmonary vessels + arteries
○ Right-sided heart failure may occur r/t pulmonary resistance
● Destruction of Bronchial Walls
○ Dilation of airway sacs (Bronchiectasis)
Inflammation → Neutrophil activity→ Interleukin-8 levels ↑ // CD8 T-lymphocyte levels ↑ // Eosinophils ↑
Dx ● Chest x-ray
○ ↑ Bronchial vascular markings, Congested lung fields, Enlarged horizontal cardiac silhouette, Evidence of
previous infection
● Pulmonary function tests
○ Normal total lung capacity (TLC), ↑ Residual volume (RV), ↓ FEV
● Arterial blood gas (ABG)
○ ↑ PaCO2 (Carbon dioxide) + ↓ PaO2 (Oxygen) (< 65 mmHg)
● ECG
○ Atrial dysrhythmias + Right ventricular hypertrophy
● Physical Examination
○ Scattered crackles, Rhonchi, Wheezes; Use of accessory muscles; Jugular vein distention; Clubbing;
Pedal/Ankle edema
Clinical Manifestations ● Overweight
● Commonly associated with emphysema
● Exertional dyspnea
● Excessive sputum
● Chronic cough (more severe in morning)
● Excess body fluids (edema, hypervolemia)
● Cyanosis (LATE SIGN)
