Topic 2: Dyspnea and Hypoxia

Lalaine M. Nicolas, MD
9/13/13

DYSPNEA
Definition of DYSPNEA
 SUBJECTIVE experience of breathing discomfort.
 Consists of qualitatively distinct sensations that vary in intensity.
 Interactions among multiple Physiological, Psychological, Social, and Environmental factors.
 May induce secondary Physiological and Behavioral responses.

How important is DYSPNEA as a symptom?

 Up to 50% of patients admitted to acute, tertiary care hospitals, up to 25% of ambulatory care
consultations.
 A complex symptom that potentially warns of a critical threat to homeostasis and frequently leads to
adaptive responses.
 Predictor of hospitalization and mortality in patients with chronic lung disease and cardiac disease.

Problems in the study of Dyspnea:

 There are no specialized dyspnea receptors.
 There is no area of the cortex that when stimulated causes dyspnea or any other respiratory sensation.
 It is difficult to define the precise physical stimulus that causes it.

Efferent and Afferent Signals That Contribute to the Sensation of Dyspnea

Figure 1. Efferent and Afferent Signals That Contribute to the Sensation of Dyspnea.
The sense of respiratory effort is believed to arise from a signal transmitted from the motor cortex to the sensory
cortex coincidently with the outgoing motor command to the ventilatory muscles. The arrow from the brain stem to
the sensory cortex indicates that the motor output of the brain stem may also contribute to the sense of effort. The
sense of air hunger is believed to arise, in part, from increased respiratory activity within the brain stem, and the
sensation of chest tightness probably results from stimulation of vagal-irritant receptors. Although afferent
information from airway, lung, and chest-wall receptors most likely passes through the brain stem before reaching
the sensory cortex, the dashed lines indicate uncertainty about whether some afferents bypass the brain stem and
project directly to the sensory cortex.

Mechanisms of Dyspnea
Motor Efferents (Feed-forward)
Sensory Afferents (Feedback)
Integration
• Increased neural output from the cortex.
• Corollary Discharge is sent to the sensory cortex.
• Chemoreceptors: hypoxemia, acute hypercapnia, acidemia
• Mechanoreceptors: bronchospasm
• J-receptors: interstitial edema
• Pulmonary vascular receptors: Changes in pulmonary artery pressure
• Metaboreceptors: changes in local biochemical milieu
• Efferent-Reafferent Mismatch
• A discrepancy between the feed-forward message to the ventilatory muscles
and the feedback from receptors increases the intensity of dyspnea.

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Anxiety
 Increase the severity of dyspnea by altering the interpretation of sensory data
o leading to patterns of breathing that heighten physiologic abnormalities in the respiratory system.

ASSESSING DYSPNEA:
1. Quality
Descriptors
Chest tightness or constriction
Increased work or effort of breathing
Air hunger, Need to breathe, Urge to breathe
Cannot get a deep breath, Unsatisfying breath
Heavy breathing, Rapid breathing, Breathing more
Pathophysiology
Bronchoconstriction (Asthma)
Interstitial edema (CHF, Myocardial Ischemia)
Airway obstruction (COPD, Moderate-Severe Asthma)
Neuromuscular disease (Myopathy, Kyphoscoliosis)
Increased drive to breathe (CHF, Pulmonary Embolism,
Moderate to Severe COPD/Asthma)
Hyperinflation (Asthma, COPD)
Restricted tidal volume (Pulmonary Fibrosis, Chest Wall
Restriction)
Deconditioning

2. Intensity (Affective Dimension)

DYSPNEA MEASURES
Sensory-Perceptual Measures
Measures of Affective Distress
Measures of Symptom Impact
• Measures what breathing feels like.
• Ratings of intensity/ sensory quality
• Visual Analog Scale, Borg Rating, Likert-type Ratings, Numerical Rating Scales
• Measures the perception of immediate unpleasantness/ judgment about the
possible consequences of what is perceived.
• Single or Multiple item scales
• Measures how breathing affects behaviors, beliefs, or values that matter to
patients or society.
• Involve multi-item scales across multiple dimensions: functional performance,
quality of life, psychosocial functioning.

Visual Analog Scales

Measures of Symptom Impact

Modified Medical Research Council (MRC) Scale
0 I only get breathless with strenuous exercise.
1 I get short of breath when hurrying on the level or walking up a slight hill.
2 I walk slower than people of the same age on the level because of breathlessness or have to stop for breath
when walking at my own pace on the level.
3 I stop for breath after walking about 100 yards or after a few minutes on the level.
4 I am too breathless to leave the house or I am breathless when dressing.

Differential Diagnosis

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Respiratory System Dyspnea
Diseases of the Airways
• Asthma
• COPD
Diseases of the Chest Wall
• Kyphoscoliosis
• Myasthenia gravis
• Guillain-Barre syndrome
• Pleural Diseases
Diseases of the Lung Parenchyma
• Pneumonia
• Interstitial lung diseases
• Occupational ILD
• Autoimmune Disorders

Cardiovascular System Dyspnea

Diseases of the Left Heart Diseases of the Pulmonary Vasculature Diseases of the Pericardium
• Coronary Artery Disease • Pulmonary thromboembolic • Constrictive Pericarditis
• Cardiomyopathies disease • Cardiac Tamponade
• Diastolic Dysfunction

Dyspnea with Normal Respiratory and Cardiovascular Systems

 Anemia
 Obesity
 Cardiovascular Deconditioning/Poor Fitness

Evaluation of Dyspnea
 Two Major Categories of Patients with Dyspnea:
o New onset of breathing discomfort for whom the underlying cause of dyspnea has not yet been
determined.
 Goal: Underlying abnormality or diagnosis?
o Those with known cardiovascular, respiratory, or neuromuscular disease who are experiencing
worsening dyspnea.
 Goal: Is there is deterioration of a known disorder?
Emergence of a new problem?

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History
Description of dyspnea • Words a patient uses to describe the dyspnea
Tempo of onset, Duration, Frequency • Sudden or Progressive over time
• Acute VS Chronic
• Intermittent VS Continuous/ Persistent
• Daily?, Several times per month/year?
Severity • Affects activities of daily living?
• Dyspnea Scales
Aggravating factors • Relation to position
• Effort-related
• Exposures
Relieving factors • Rest
• Position
• Medications
Associated Symptoms • Cough, phlegm production, wheezing, fever, chest/back pains
Risk factors • Smoking, Occupational
• Previous illnesses, Family history

Physical Examination
General Appearance Level of consciousness, ambulation, Color, Signs of respiratory distress,
Ability to speak
Vital Signs Tachypnea, tachycardia, Hypoxemia (O2 desaturation by Oximetry),
Pulsus paradoxus
Chest Absent or decreased breath sounds, Wheezing, Crackles, Rhonchi
Cardiac Exam JVP elevation, Apex beat displaced, Precordial impulse, Gallop, Murmurs
Extremities Weak/ bounding pulses, Edema, Cyanosis,

Diagnostic Work-up
Chest X-Ray • Cardiac size
• Infiltrates- pneumonia, PTB, ILD
• Nodules, Mass lesions
• Evidence of hyperinflation: flattening of the diaphragm, widening
of intercostal spaces
• Pleural diseases
ECG • Presence of ischemia, arrythmias, evidence of hypertrophy
Echocardiogram • Assess left ventricular function
• Assess pulmonary artery pressure
Pulmonary Function Testing • Lung function
• Obstructive VS Restrictive lung diseases
CT Scan • Pulmonary nodules and mass
CT Angiogram • Bronchiectasis, Abscess
• Pulmonary embolism, ILD
Blood Tests CBC- Anemia
Uremia
Thyroid Function Tests
Cardiopulmonary Exercise Test Respiratory Problem
• Patient achieves predicted maximal ventilation
• Increased dead space
• Hypoxemia
• Bronchospasm
Cardiovascular Problem
• HR > 85% max predicted
• Anaerobic threshold occurs early
• Excessively high BP/ Decreases significantly
• O2 sat falls
• ECG abnormalities

Treatment
Treat underlying
Supplemental Oxygen
problem

Pulmonary
Pharmacologic Therapy
Rehabilitation

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HYPOXIA
Definition of Terms
Hypoxia insufficient oxygenation of the tissues
Hypoxemia implies a failure of the respiratory system to oxygenate arterial blood
Anoxia lack of oxygen at the tissue level
PAO2 Partial pressure of alveolar oxygen
PaO2 Partial pressure of arterial oxygen
FIO2 Fractional concentration of inspired Oxygen

Responses to Hypoxia
 Marked alteration in gene expression: production of transcription factors mediated by hypoxia- inducible
factors (HIFs)→ activate genes that produce angiogenic factors and erythropoietin.
 Pasteur effect: Switch from aerobic to anaerobic metabolism.
 Decreased ATP production → Cell membrane depolarization leads to uncontrolled Ca++ influx and
activation of Ca++ dependent phospholipases and proteases → Cell swelling and cell death
 Cessation of aerobic metabolism, exhaustion of high-energy intracellular stores, cellular dysfunction, and
death.

Responses of Organ Systems to Hypoxia

Respiratory System • Stimulation of carotid and aortic baroreceptors result in increased rate and
depth of ventilation.
• Pulmonary arterial constriction shunts blood away from poorly ventilated
portions toward better ventilated portions of the lung.
Cardiovascular System • Reflex activation of the sympathetic nervous system by both autonomic and
humoral mechanisms, resulting in tachycardia and increased cardiac output.
• Peripheral vascular resistance decreases through local autoregulatory
mechanisms, maintaining blood pressure.
CNS • Acute hypoxia: decreased intellectual capacity, impaired judgment, motor
intoxication.
• Prolonged hypoxia: Confusion, restlessness, stupor coma and death.

Causes of Hypoxia
Respiratory Hypoxia
Low FIO2  Hypoxia secondary to high altitude
 At 3000m (10,000 ft) the decreased FIO2 leads to decreased alveolar PO2 – High
altitude Illness
 At ≥ 5000, unacclimatized individuals cease to be able to function normally.
Hypoventilation  Causes hypoxemia by reducing the alveolar PO2 in proportion to the build-up of
CO2 in the alveoli.
Diffusion Impairment  Interstitial fibrosis/edema
Shunting  Perfusion of nonventilated portions of the lung.
 The blood leaving the region has the same low PO2 and high PCO2 as mixed
venous blood (Intrapulmonary right to left shunting)
 Atelectasis, Pulmonary arteriovenous connections

Ventilation-Perfusion Mismatch: When ventilation is not in balance with perfusion, O2 exchange is compromised.

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Causes of Hypoxia
Right – to- left Extrapulmonary Shunting
Anemic Hypoxia
Carbon Monoxide Intoxication
Circulatory Hypoxia
Specific Organ Hypoxia/ Ischemic
Hypoxia
Increased O2 requirements
Improper Oxygen Utilization/ Histotoxic
Hypoxia
 Cardiovascular abnormality
o Interatrial septal defect permits large amounts of
unoxygenated venous blood to bypass the pulmonary
capillaries and dilute the oxygenated blood in the
systemic arteries.
 Manifests with chronic hypoxemia and cyanosis.
 Decrease in the amount of functioning Hb
 Decreased Hb or erythrocyte production
 Production of abnormal Hb or RBCs
 Pathologic destruction of erythrocytes
 Decreased O2 content when both PAO2 and PaO2 are normal.
 Carbon Monoxide is formed by incomplete combustion of
Carbon
 It reacts with Hb to form carboxyhemoglobin (COHb), the affinity
of Hb for CO is 210x its affinity for O2
 The cherry-red color of COHb is visible in the skin, nailbeds and
mucous membranes.
 Death results when 70-80% of the circulating Hb is converted to
COHb
 Reduced tissue perfusion and greater tissue extraction.
 Seen in patients with heart failure and most forms of shock (Septic
shock, Hypovolemic Shock)
 The PaO2 is normal but venous and tissue PO2 are reduced,
hence, increased arterial-mixed venous O2 gradient.
 Decreased perfusion to a particular organ/ vascular bed
 Arterial obstruction eg, localized atherosclerosis
 Venous obstruction- resultant expansion of interstitial fluid causing
arteriolar compression and subsequent reduction of arterial inflow
 Localized vasoconstriction (Raynaud’s phenomenon)
 There is increased O2 consumption of tissues without
corresponding increase in perfusion
o Eg. Fever, Thyrotoxicosis, Exercise
 Poisoning of the cellular machinery that uses O2 to produce
energy
o CYANIDE poisoning- binds to cytochrome oxidase in the
respiratory chain and effectively blocks oxidative
phosphorylation
 Alveolar and arterial PO2 are normal, Venous PO2 and O2
content are elevated because O2 is not utilized.

Adaptation to Hypoxia
 Stimulation of peripheral chemoreceptors in the carotid and aortic bodies and central chemoreceptors in
the brainstem- Increased ventilation, Respiratory alkalosis
 Increased production of lactic acid- results in metabolic acidosis
 Cerebrovascular resistance decreases and cerebral blood flow increases in an attempt to maintain O2
delivery to the brain.
 Diffuse systemic vasodilation increases cardiac output.
 Increased Hb concentration and erythrocytosis.

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CYANOSIS
 Bluish discoloration of the skin and mucous membranes.
o Increased quantity of reduced Hb (deoxygenated Hb)
o Increased quantity of Hb derivatives (Methemoglobin, Sulfhemoglobin)

Causes of Cyanosis

CENTRAL CYANOSIS PERIPHERAL CYANOSIS

Decreased arterial oxygen saturation Reduced cardiac output
• Decreased atmospheric pressure- high altitude Cold exposure
• Impaired pulmonary function Redistribution of blood flow from extremities
• Alveolar hypoventilation Arterial obstruction
• Ventilation-Perfusion mismatch Venous obstruction
• Impaired O2 diffusion
Anatomic shunt
• Certain types of Congenital heart diseases
• Pulmonary arteriovenous fistulas
• Multiple small intrapulmonary shunts
• Hemoglobin with low affinity for O2
Hemoglobin abnormalities
• Methemoglobinemia
• Sulfhemoglobinemia
• Carboxyhemoglobinemia

Approach to Patients with Cyanosis

Time of onset?

Central VS Peripheral?

Is there clubbing?

PaO2? SaO2?
Spectroscopic exam?
CLUBBING
 Selective bulbous enlargement of the distal segments of the fingers and toes due to proliferation of
connective tissue, particularly on the dorsal surface.
 Increased sponginess of the soft tissue at the base of the clubbed nail.
 Mechanism: Secondary to humoral substances that cause dilation of the vessels of the distal digits as well
as growth factors released from unfragmented platelet precursors in the digital circulation.

Causes of Clubbing
Hereditary
Idiopathic
Acquired Congenital heart disease, Infective endocarditis, Primary and metastatic lung cancer, Bronchiectasis,
Asbestosis, Sarcoidosis, Lung abscess, Cystic fibrosis, Tuberculosis, Mesothelioma, Inflammatory bowel
disease, Hepatic cirrhosis

Please read at your own risk! Go batch 2016!

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