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Respiration, the act of breathing, is unique in that, of all the vital functions, it alone is regulated not only by automatic centers located in the brainstem but also by voluntary signals initiated in the cortex. Insofar as individuals have some control over their breathing, sensations arising from respiratory activity affect the rate and pattern of breathing as well as the individual's functional status.

Psychological and cultural factors may influence the reaction to a sensation, e.g., a stoic individual may deny respiratory discomfort and push beyond the limitations experienced by another person more sensitive to bodily messages.

The context in which a sensation occurs can also impact the perception of the event. The sensation experienced by an individual during maximal exercise will evoke very different reactions than the same sensation occurring at rest.

Dyspnea- Subjective experience of breathing

discomfort that consists of qualitatively distinct sensations that varies in intensity.

- Interactions among multiple physiological, psychological, social and environmental factors, and may induce secondary physiological and behavioural responses.

CaseDuring a routine physical examination, a man tells his doctor that his wife has commented that he is short of breath when he talks on the telephone. The patient indicates that he is unaware of any breathing discomfort.

*Does this patient have dyspnea?No. Dyspnea is a symptom. It is present if, and only if, the patient perceives breathing discomfort.

The symptom must be distinguished from signs of respiratory distress such as increased ventilation, use of accessory muscles of ventilation, an inability to speak in full sentences because of the need to

take many breaths, a rapid respiratory rate, or wheezing.

Mechanisms of Dyspnea

Sensory Afferents

Subject: MedicineTopic: Dyspnea and HypoxiaLecturer:Transcriptionist: BellasPages:9

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The sensation of dyspnea seems to originate with the activation of sensory systems involved with respiration. Sensory information is, in turn, relayed to higher brain centers where central processing of respiratory-related signals and contextual, cognitive, and behavioral influences shape the ultimate expression of the evoked sensation.

Anxiety- Increase the severity of dyspnea- May alter interpretation of sensory data- Abnormal patterns of breathing

Summary of the Pathophysiology of Dyspnea• Neuro-mechanical/ Efferent-reafferent

Dissociation – mismatch between central respiratory motor activity and incoming afferent information from receptors in the airways, lungs, and chest wall structures.

• Heightened Ventilatory Demand – increase in respiratory motor output and a corresponding increase in the sense of effort.

• Respiratory Muscle Abnormalities –Weakness or mechanical inefficiency of the respiratory muscles results in a mismatch between central respiratory motor output and achieved ventilation.

The afferent feedback from peripheral sensory receptors may allow the brain to assess the effectiveness of the motor commands issued to the ventilatory muscles, i.e., the appropriateness of the response in terms of flow and volume for the command. When changes in respiratory pressure, airflow, or movement of the lungs and chest wall are not appropriate for the outgoing motor command, the intensity of dyspnea is heightened. In other words, dissociation between the motor command and the mechanical response of the respiratory system may produce a sensation of

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respiratory discomfort. The theory has been generalized to include not only information arising in the ventilatory muscles, but information emanating from receptors throughout the respiratory system and has been termed "neuro-mechanical", or "efferent-afferent dissociation".

Patients with a mechanical load on the respiratory system, either resistive or elastic, or respiratory muscle abnormalities will have dissociation between the efferent and afferent information during breathing. The mismatch of neural activity and consequent mechanical or ventilatory outputs may contribute to the intensity of dyspnea under these conditions.

Heightened ventilatory demand. It is regularly observed, both in normal individuals and in patients with lung disease, in which the intensity of the dyspnea increases progressively with the level of ventilation during exercise. There are, however, important contextual influences on the interpretation of respiratory-related sensations. Thus, symptoms of shortness of breath are more likely to be reported when hyperpnea occurs at rest and cannot be accounted for by an increase in exertion or physical activity.

ASSESSING DYSPNEA Quality

Determine quality of discomfort- Patient’s description “in his own

words”- Dyspnea questionnaires- First, subjects should be asked to

describe in their own words the nature of their "breathing discomfort." A symptom can only be described by the person who experiences it.

- Second, we ask the subject to look at the list of phrases on the dyspnea questionnaire and to place a check-mark next to each of the phrases that applies to the breathing discomfort experienced during the circumstances under study.

Intensity Determine sensory intensity

- Modified Borg Scale- Visual Analog Scale- The Baseline Dyspnea Index- Chronic Respiratory Disease

Questionnaire- Consider the ways in which the

intensity of sensations may vary with time.

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Visual Analogue Scale

Baseline Dyspnea IndexChronic Respiratory Disease Questionnaire (St. George’s Respiratory Questionnaire)

Affective Dimension Patient’s perception of a sensation is

“unpleasant” Emotional or behavioural response to

the discomfort.

Differential Diagnosis

*refer to powerpoint

Dyspnea is often secondary to a respiratory or cardiovascular problem.Respiratory Problems

Gas exchange problem – problem is in the alveolo-capillary area

Ventilatory Pump – meaning the thoracic cage and respiratory muscles

Respiratory Control Centers

Cardiovascular Low Output Normal High Output

Algorithm for the Evaluation of the Patient with Dyspnea History

o When taking the history of a patient complaining dyspnea, get a good description of dyspnea

Describe in his own words, if not use the dyspnoeic questionnaire

Onset – acute or insiduous Duration – how long has been

the patient experiencing this problem

Frequency – continuous or intermittent

Conditions in which dyspnea occurs

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Effect of activity, position, infections, emotional state and environmental stimuli

Quantify the intensity Associated symptoms How the dyspnea affects the

patient’s life Associative affective state

- Anxiety, panic depression, etc.

Risk factors- PMH- Family History- Occupational Risk

Physical Examination of Patient If the diagnosis is not evident, you must do one

diagnostic test: CHEST RADIOGRAPHY

Dyspnea on exertion

Dyspnea that occurs related to physical activity; may be indicative of disease when it occurs at a level of activity that is usually tolerated.-Think of possible chronic lung diseases such as COPD or even cardiovascular diseases such as myocardial ischemia

Orthopnea Sensation of breathlessness in the recumbent position, relieved by sitting or standing.-more on cardiovascular causes of dyspnea

Paroxysmal Nocturnal Dyspnea (PND)

Sensation of shortness of breath that awakens the patients, often after 1-2 hours of sleep; usually relieved in the upright position-more on cardiovascular causes of dyspnea

Trepopnea Dyspnea that occurs in one lateral decubitus position as opposed to the other.-possibly pleural effusion

Platypnea Breathlessness that occurs in the upright position and is relieved with recumbency.

Physical ExaminationUpon entry of patient, Check:General appearance

ambulatory? Wheelchair-bourne? Conscious? confused? drowsy? Color? (pale, cyanotic) Can speak in full sentences? Signs of respiratory distress? (orthopneic,

use of accessory muscles of respiration) Vital Signs

Tachypneic? Apneic? Tachycardic? Pulsus paradoxus? Oximetry-evidence of desaturation?

Chest and Lungs

Symmetry of lung expansion Abnormal percussion notes Adventitious Sounds Are the breath sounds normal?

Cardiac JVP elevated? Precordial impulse? Abnormal heart sounds? Gallop? Murmur?

Extremities Edema? Cyanosis? Clubbing?

Other extrapulmonary signs

Chest RadiographyBy doing it, you can see the

size of the heart if there are infiltrates Possible masses in the lungs Pneumothorax, pleural effusion Hyperinflation

*more or less will give you an idea on the possible diagnosis-should have a working diagnosis

(please refer to the PPT for a clearer view)*if after doing ECG/Pulmonary function testing,etc, you still don’t have a diagnosis, you have to do:

Cardiopulmonary exercise test (CPET) A patient exercises to the point of

exhaustion then you measure the: The maximum oxygen consumption

at peak exercise (VO2). The anaerobic threshold (the point

at which the exercising muscles stop receiving oxygen, and lactic acid is accumulated).

The maximal heart rate achieved. The maximal breathing rate.

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The efficiency of the heart and the lungs to mobilize during exercise.

Interpretation of CPET Pulmonary - if at peak exercise, predicted

maximal ventilation is achieved but increase dead space or hypoxemia is noted or patients develop bronchospasm.

Cardiac- if HR is > 85% predicted maximum, anaerobic threshold occurs early, excessively high or low BP, O2 pulse falls or ischemic change in ECG

Treatment of DyspneaAfter obtaining diagnosis,

Main Goal: Correct the underlying problem, if possible.

o If not, lessen the intensity of dyspnea and its effect on the patient’s quality of life.

Supplemental O2- if O2 sat ≤ 90% Pulmonary rehabilitation will help

Hypoxia

Webster’s Dorland’s Stedman’s

HYPO

XIA

A deficiency in the amount of oxygen that reaches the tissues of the body.

Reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of tissue by blood.

Decrease below normal levels of oxygen in inspired gases, arterial blood, or tissue, short of anoxia

ANO

XIA

An abnormally low amount of oxygen in the body tissues.

A total lack of oxygen supply to the tissues.

Absence or almost complete absence of oxygen from inspired gases, arterial blood, or tissues

HYPO

XEMIA

Inadequate oxygenation of the blood.

Deficient oxygenation of the blood.

Subnormal oxygen of arterial blood.

Hypoxia: decreased oxygen availability to the cells

Effects of Hypoxia Increased anaerobic glycolyis In severe case: Cell membrane

depolarization uncontrolled Ca2+

influx activates Ca2+dependent

phospolipase & proteases cell swelling & cell necrosis

Systemic arterioles dilation Enhanced erythrocyte production,

subsequently, polycythemia

Pulmonary arterial constriction increase pulmonary vascular resistance & right ventricular afterload

CNS effects of hypoxia Vasodilatation and increased blood flow to

the brain Dilatation of the pial vessels

Impaired judgment Motor incoordination Clinical picture resembling acute alcoholism Headache Dizziness Patients with HACE (high altitude cerebral

edema): severe headache, papilledema, coma

If the centers of the brainstem affected-patients may go to respiratory failure

Causes of Hypoxia 1. Inadequate oxygenation of the blood in the

lungs because of extrinsic reasons• Deficiency of oxygen in the atmosphere

2. Pulmonary disease• Hypoventilation caused by increased

airway resistance or decreased pulmonary compliance, neuromuscular disorders

• Abnormal alveolar ventilation-perfusion ratio

• Diminished respiratory membrane diffusion

• Intrapulmonary right-to left-shunting3. Venous-to-arterial shunts (right-to-left cardiac shunts) 4. Inadequate O2 transport to the tissues by the blood

• Anemia or abnormal Hb • Generalized circulatory deficiency• Localized circulatory deficiency

(peripheral, cerebral, coronary vessels)• Tissue edema

5. Inadequate tissue capability of using O2• Poisoning of cellular oxidation enzymes

(Cyanide)

results to

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• Diminished cellular metabolic capacity for using O2 (Toxicity, Vit deficiency)

Hypoxia secondary to high altitude High altitude illness- As one ascends to

3000m (10,000ft), the reduction of the O2 content of inspired air (FIO2) leads to a decrease in alveolar PO2 to about 60mmHg

At higher altitudes, O2 arterial saturation further declines rapidly

*The PO2 in the air we breathe is 0.2093 x barometric pressure as we go higher barometric pressure

decreases PO2 in the air also decreases

Respiratory Hypoxia

The Oxyhemoglobin dissociation curve describes the non-linear tendency for oxygen to bind to hemoglobin: below a SaO2 of 90%, small differences in hemoglobin saturation reflect large changes in PaO2 If hypoxia is secondary to respiratory causes,

The O2-Hb curve is displaced to the right with greater quantities of O2 released at any level of tissue PO2

Causes of Respiratory Hypoxia Ventilation-Perfusion Mismatching (V-Q

mismatch)o Either inadequate ventilation or

perfusiono The most common cause of respiratory

hypoxia is VQ mismatch resulting from perfusion of poorly ventilated alveoli eg, ARDS, severe pneumonia. This can be corrected by inspiring 100% O2.

Intrapulmonary right-to-left shunt

o Shunting of blood across the lungs from the pulmonary arterial to the venous bed by perfusion of nonventilated portions of the lung eg. Pulmo embolism, atelectasis. This time of hypoxemia is not corrected by even 100% FIO2.

Hypoventilationo Impaired respiratory drive carotid

body dysfunction, trauma, brainstem disorders

o Defective respiratory neuromuscular system high cervical trauma, myasthenia gravis, muscular dystrophy

o Impaired ventilator apparatus kyphoscoliosis, obesity hypoventilation, COPD, laryngeal and trachel stenosis

Diffusion Defectso Pulmonary fibrosiso Pulmonary edema

Normal: The diffusion capacity depends on the thickness of the alveolar wall, the area available for gas exchange and the partial pressure difference between the two sides. In PF and PE there is thickening of the alveolar wall.

Hypoxia secondary to right-left Extrapulmonary ShuntingDeoxygenated blood goes to the left heart and back into the circulation without passing the lungs. The PaO2 cannot be restored to normal even with inspiration of 100% O2

Due to congenital heart diseaseo Tetralogy of Falloto Transposition of Great Vesselso Eisenmenger’s syndrome

Cannot be restored by 100% O2 inhalation

Anemic Hypoxia Decrease hemoglobin results in decreased

O2 carrying capacity of blood. Normal PaO2 but decrease PO2 and

saturation of venous bloodCirculatory Hypoxia

Seen in patients with heart failure and some types of shock such as hypovolemic shoch and septic shock

Reduced tissue perfusion and greater tissue O2 extraction

o Normal PaO2 but decrease venous & tissue PO2

Increased arterial-mixed venous O2

difference or (a-v) gradient

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Occurs in heart failure & shock

Specific Organ Hypoxia Arterial obstruction (atherosclerosis)

decreased perfusion to localized areas Vasoconstriction (Raynaud’s phenomenon,

CHF, hypovolemic shock) attempting to maintain adequate perfusion to more vital organs

Venous obstruction leads to arterial compression leads to local swelling

Edema increases the distance through which O2 must diffuse before it reaches the cells

Carbon Monoxide Intoxication Carbon monoxide binds to hemoglobin

Carboxyhemoglobin is unavailable for O2

transport

Shift Hb-O2 dissociation curve to the left

Hypoxia sec to Increased O2 Requirements Due to elevated metabolic rate (fever,

thyrotoxicosis) In exercise, hypoxia occurs if the

following compensatory mechanism is exceeded:

1. increase cardiac output & ventilation2. preferential blood circulation in exercising muscles3. increase O2 extraction and widen a-v O2 difference

4. decrease pH, shifting Hb-O2 curve to right

Skin is flushed & warm and no cyanosis

Adaptation to Hypoxia Stimulation of the carotid and aortic bodies

in the respiratory center and brainstem increased ventilationrespiratory alkalosis

Lactic acidosis Diffuse systemic vasodilatation

increased cardiac output Increased Hb concentration and increased

number of RBCs in the circulating bloodpolycythemia

Cyanosis Bluish discoloration of the skin and mucous

membranes resulting from an increased quantity of reduced Hb, or of Hb derivatives, in the small blood vessels of those areas

Increase in the quantity of venous blood (result of dilatation of the venules and venous ends of the capillaries)

Reduction in the SaO2 in the capillary blood Concentration of reduced Hb in capillary

blood › 40g/L Lips, nail beds, ears, malar eminences,

mucous membranes are involved Degree of cyanosis modified by the color

and thickness of the skin and the state of the cutaneous capillaries

Central VS Peripheral Cyanosis Central-

the SaO2 is reduced or an abnormal Hb derivative is present

Mucous membranes and skin are both affected

Peripheral- Slowing of blood flow and

abnormally great extraction of O2 from normally saturated arterial blood

Results from vasoconstriction and diminished peripheral blood flow

Mucous membranes of the oral cavity and beneath the tongue may be spared

Combined central and peripheral (it can also appear together)

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Approach to the patient with Cyanosis1. Time of Onset2. Central Vs. Peripheral3. Presence of Clubbing – usually occurs in central

a. clubbing does not occur in peripheral4. Determination of the PaO2 and SaO2

Spectroscopic examination of the blood: Abnormal Types of Hb

Clubbing Selective bullous 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 nail

Secondary to a humoral substance that causes dilation of the vessels of the fingertip

Causes of clubbing Hereditary, idiopathic or acquired Diseases associated with clubbing:

Cyanotic congenital heart disease Infective endocarditis Pulmonary diseases ( lung cancer,

bronchiectasis, lung abscess, cystic fibrosis, mesothelioma)

GI diseases (IBD, hepatic cirrhosis)

Occupational (jackhammer operator)

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“Get rid of all bitterness, rage and anger, brawling and slander, along with every form of malice. Be kind and compassionate to one another, forgiving each other, just as in Christ God forgave you. “

Ephesians 4: 31-32