Alterations in Respiratory

Functions
Sophie Tatishvili
Hypothetical model for integration of sensory inputs in the production of dyspnea. Afferent information from
the receptors throughout the respiratory system projects directly to the sensory cortex to contribute to primary
qualitative sensory experiences and to provide feedback on the action of the ventilatory pump. Afferents also
project to the areas of the brain responsible for control of ventilation. The motor cortex, responding to input
from the control centers, sends neural messages to the ventilatory muscles and a corollary discharge to the
sensory cortex (feed-forward with respect to the instructions sent to the muscles). If the feed-forward and
feedback messages do not match, an error signal is generated and the intensity of dyspnea increases. An
increasing body of data supports the contribution of affective inputs to the ultimate perception of unpleasant
respiratory sensations. (Adapted from MA Gillette, RM Schwartzstein, in SH Ahmedzai, MF Muer [eds].
Supportive Care in Respiratory Disease. Oxford, UK, Oxford University Press, 2005.)
Harrison's Principles of Internal Medicine, 18e
 Modified Borg scale dyspnea score. This scale consists of both verbal
(10) and numerical (12) descriptions for dyspnea assessment. Patients
are asked to tick the boxes that reflect their dyspnea perception best
July 2013 Supportive Care in Cancer 21(11) DOI
10.1007/s00520-013-1895-3
Methods indirectly assess dyspnea and may be affected by
nonrespiratory factors, such as leg arthritis or weakness

Baseline Dyspnea Index

Chronic Respiratory Disease Questionnaire
Harrison's Principles of Internal Medicine, 18e
 Association of Qualitative Descriptors, Clinical Character
istics, Pathophysiologic Mechanisms of Shortness of BREATH

Harrison's Principles of Internal Medicine, 18e

Mechanisms of Dyspnea in Common Disease

Harrison's Principles of Internal Medicine, 18e

 Common Causes of Noncardiogenic Pulmonary
Edema
Direct Injury to Lung
Chest trauma, pulmonary contusion
Aspiration Smoke inhalation
Pneumonia
Oxygen toxicity
Pulmonary embolism, reperfusion
Hematogenous Injury to Lung
Sepsis
Pancreatitis
Nonthoracic trauma
Leukoagglutination reactions
Multiple transfusions
Intravenous drug use (e.g., heroin) Cardiopulmonary
bypass
Possible Lung Injury Plus Elevated Hydrostatic
Pressures
High-altitude pulmonary edema
Neurogenic pulmonary edema
Reexpansion pulmonary edema Harrison's Principles of Internal Medicine, 18e
https://www.med-ed.virginia.edu/courses/rad/cxr/pathology2chest.html
Kerley B Lines

https://www.med-ed.virginia.edu/courses/rad/cxr/pathology2chest.html
Acute Pulmonary Edema NEJM 2005
Acute Pulmonary Edema NEJM 2005
Causes of Impaired Cough
Decreased expiratory-muscle strength
Decreased inspiratory-muscle strength
Chest wall deformity Impaired glottic closure or
Tracheostomy
Tracheomalacia
Abnormal airway secretions
Central respiratory depression (e.g., anesthesia,
sedation, or coma)

Harrison's Principles of Internal Medicine, 18e

Respiratory Hypoxia
Ventilationperfusion mismatch Causes
Hypoventilation
(intrapulmonary right-to-left shunting)
Hemoglobin-oxygen dissociation curve.
of HypoxiaThe hemoglobin tetramer can bind up to
four molecules of oxygen in the
ironcontaining sites of the heme
molecules. As oxygen is bound, 2,3-
bisphosphoglycerate (2,3-BPG) and
carbon dioxide (CO2 ) are expelled. Salt
bridges are broken, and each of the
globin molecules changes its
conformation to facilitate oxygen
binding. Oxygen release to the tissues is
the reverse process, with salt bridges
being formed and 2,3-BPG and CO2
bound. Deoxyhemoglobin does not bind
oxygen efficiently until the cell returns to
conditions of higher pH, the most
important modulator of O2 affinity (Bohr
effect). When acid is produced in the
tissues, the dissociation curve shifts to
the right, facilitating oxygen release and
CO2 binding. Alkalosis has the opposite
effect, reducing oxygen delivery
 Types of Hypoxia
Hypoxia Secondary to High Altitude
Hypoxia Secondary to Right-to-Left Extrapulmonary Shunting
Anemic Hypoxia
Carbon Monoxide (CO) Intoxication
Circulatory Hypoxia
Specific Organ Hypoxia
Increased O2 Requirements
Improper Oxygen Utilization - histotoxic hypoxia
 Causes of Cyanosis
Central Cyanosis
Decreased arterial oxygen saturation
• Decreased atmospheric pressure—high altitude
• Impaired pulmonary function
Alveolar hypoventilation
Inhomogeneity in pulmonary ventilation and perfusion (perfusion of hypoventilated
alveoli)
Impaired oxygen diffusion
Anatomic shunts
•Certain types of congenital heart disease
•Pulmonary arteriovenous fistulas Multiple small intrapulmonary shunts
•Hemoglobin with low affinity for oxygen
Hemoglobin abnormalities
Methemoglobinemia—hereditary, acquired
Sulfhemoglobinemia—acquired
Carboxyhemoglobinemia (not true cyanosis)
Peripheral Cyanosis
Reduced cardiac output
Cold exposure
Redistribution of blood flow from extremities
Arterial obstruction
Venous obstruction

Harrison's Principles of Internal Medicine, 19e

Elastic recoil pressure of the lung - a positive transmural pressure difference
between alveolar gas and its pleural surface to stay lungs inflated;
act on the chest
wall to generate
the equivalent of
positive pressure
across the lungs
and passive chest
wall,

generate the equivalent

of negative
transrespiratory pressure
DOI: 10.13140/RG.2.2.21169.02401
 Flow-volume loops. A. Normal. B. Airflow obstruction. C. Fixed central
airway obstruction. RV, residual volume; TLC, total lung capacity.

Harrison's Principles of Internal Medicine, 19e

Harrison's Principles of Internal Medicine, 19e