Subject: Medicine Topic: Dyspnea and Hypoxia Lecturer: Transcriptionist: Bellas Pages:9

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. Case During 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

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

SY 2011-2012

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 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 "neuromechanical", 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 - Patients 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 checkmark 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.

Affective Dimension Patients perception of a sensation is unpleasant Emotional or behavioural response to the discomfort.

Differential Diagnosis

Visual Analogue Scale *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 (St. 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 Effect of activity, position, infections, emotional state and environmental stimuli Quantify the intensity 4

Baseline Dyspnea Index Chronic Respiratory Disease Questionnaire Georges Respiratory Questionnaire)

Associated symptoms How the dyspnea affects the patients 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 Sensation of shortness of Nocturnal breath that awakens the Dyspnea patients, often after 1-2 hours (PND) 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 Breathlessness that occurs in Platypnea the upright position and is relieved with recumbency. Physical Examination Upon 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 Radiography By 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 dont 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.

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

In severe case: Cell membrane depolarization uncontrolled Ca2+ influx activates Ca2+dependent phospolipase

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 Dyspnea After obtaining diagnosis, Main Goal: Correct the underlying problem, if possible. o If not, lessen the intensity of dyspnea and its effect on the patients quality of life. Supplemental O2- if O2 sat 90% Pulmonary rehabilitation will help Hypoxia

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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 results to 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

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

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

Stedmans

An abnormally low amount of oxygen in the body tissues.

Inadequate oxygenation of the blood.

Decrease below normal levels of oxygen in inspired gases, arterial blood, or tissue, short of anoxia A total lack of Absence or oxygen supply almost to the tissues. complete absence of oxygen from inspired gases, arterial blood, or tissues Deficient Subnormal oxygenation oxygen of of the blood. arterial blood.

Hypoxia: decreased oxygen availability to the cells Effects of Hypoxia Increased anaerobic glycolyis

HYPOXIA ANOXIA HYPOXEMIA

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-shunting 3. 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) 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

lung eg. Pulmo embolism, atelectasis. This time of hypoxemia is not corrected by even 100% FIO2. Hypoventilation o 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 Defects o Pulmonary fibrosis o 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 Shunting Deoxygenated 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 disease o Tetralogy of Fallot o Transposition of Great Vessels o Eisenmengers syndrome Cannot be restored by 100% O2 inhalation

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 perfusion o 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

Anemic Hypoxia Decrease hemoglobin results in decreased O2 carrying capacity of blood. Normal PaO2 but decrease PO2 and saturation of venous blood Circulatory 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 Occurs in heart failure & shock Specific Organ Hypoxia Arterial obstruction (atherosclerosis) decreased perfusion to localized areas

Vasoconstriction (Raynauds 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

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)

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 & ventilation 2. preferential blood circulation in exercising muscles 3. 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

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

Approach to the patient with Cyanosis 1. Time of Onset 2. Central Vs. Peripheral 3. Presence of Clubbing usually occurs in central a. clubbing does not occur in peripheral 4. 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) __________END OF TRANSCRIPTION____________ 9