DYSPNOEA PowerPoint PPT Presentation

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Definition. Dyspnea refers to the sensation of difficult or uncomfortable breathing when the patient becomes aware of his own breathing. It is a subjective experience perceived and reported by an affected patient.Dyspnea on exertion (DOE) may occur normally, but is considered indicative of disease

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2. Definition Dyspnea refers to the sensation of difficult or uncomfortable breathing when the patient becomes aware of his own breathing. It is a subjective experience perceived and reported by an affected patient. Dyspnea on exertion (DOE) may occur normally, but is considered indicative of disease when it occurs at a level of activity that is usually well tolerated Dyspnea should be differentiated from tachypnea, hyperventilation, and hyperpnea, which refer to respiratory variations regardless of the patient’s subjective sensations. Tachypnea is an increase in the respiratory rate above normal Hyperventilation is increased minute ventilation relative to metabolic need

3. Hyperpnea is a disproportionate rise in minute ventilation relative to an increase in metabolic level. These conditions may not always be associated with dyspnea Orthopnea is the sensation of breathlessness in the recumbent position, relieved by sitting or standing. Paroxysmal nocturnal dyspnea (PND) is a sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position Two uncommon types of breathlessness are trepopnea and platypnea Trepopnea is dyspnea that occurs in one lateral decubitus position as opposed to the other. Platypnea refers to breathlessness that occurs in the upright position and is relieved with recumbency

4. Pathophysiology Spontaneous respiration is controlled by neural and chemical mechanisms. At rest, an average 70 kg person breathes 14to 16 times a minute with a tidal volume of about 500 ml. A normal individual is not aware of his or her respiratory effort until ventilation is doubled, and dyspnea is not experienced until ventilation is tripled. An abnormally increased muscular effort is now needed for the process of inspiration and expiration. The experience of dyspnea likely results from a complex interaction between chemoreceptor stimulation, mechanical abnormalities in breathing, and the perception of those abnormalities by CNS Because dyspnea is a subjective experience, it does not always correlate with the degree of physiologic alteration

5. Campbell and Howell (1963) have formulated the "length–tension inappropriateness theory," which states that the basic defect in dyspnea is a mismatch between the pressure (tension) generated by respiratory muscles and the tidal volume (change of length) that results. Whenever such disparity occurs, the muscle spindles of the intercostal muscles transmit signals that bring the act of breathing to the conscious level. J-receptors located in the alveolar interstitium and supplied by unmyelinated fibers of the vagus nerve, are stimulated by pulmonary congestion. Because dyspnea is a subjective experience, it does not always correlate with the degree of physiologic alteration Other theories that have been proposed to explain dyspnea include acid-base imbalance, CNS mechanisms, decreased breathing reserve, increased work of breathing, fatigue of respiratory muscles, increased oxygen cost of breathing, dyssynergy of intercostal muscles and the diaphragm, and abnormal respiratory drive.

6. Orthopnea is caused by pulmonary congestion during recumbency. In the horizontal position there is redistribution of blood volume from the lower extremities and splanchnic beds to the lungs. In normal individuals this has little effect, but in patients in whom the additional volume cannot be pumped out by the left ventricle because of disease, there is a significant reduction in vital capacity and pulmonary compliance with resultant shortness of breath. Additionally, in patients with congestive heart failure the pulmonary circulation may already be overloaded, and there may be reabsorption of edema fluid from previously dependent parts of the body Pulmonary congestion decreases when the patient assumes a more erect position, and this is accompanied by an improvement in symptoms.

7. Paroxysmal nocturnal dyspnea may be caused by mechanisms similar to those for orthopnea. The failing left ventricle is suddenly unable to match the output of a more normally functioning right ventricle; this results in pulmonary congestion. Additional mechanisms include decreased responsiveness of the respiratory center in the brain and decreased adrenergic activity in the myocardium during sleep. Dyspnea on exertion is caused by failure of the left ventricular output to rise during exercise with resultant increase in pulmonary venous pressure. In cardiac asthma, bronchospasm is associated with pulmonary congestion and is probably precipitated by the action of edema fluid in the bronchial walls on local receptors

8. Trepopnea may occur with asymmetric lung disease when the patient lies with the more affected lung down because of gravitational redistribution of blood flow. It has also been reported with heart disease when it is probably caused by distortion of the great vessels in one lateral decubitus position versus the other. Platypnea was originally described in chronic obstructive pulmonary disease and was attributed to an increased wasted ventilation ratio in the upright position. Mostly seen in b/l lower lobe disease due to poor V/Q mismatch Platypnea in association with orthodeoxia (arterial deoxygenation in the upright position) has been reported in several forms of cyanotic congenital heart disease It has been proposed that this is precipitated by a slight decrease in systemic blood pressure in the upright position, resulting in increased right-to-left shunting

9. Main Physiologic Components of Dyspnea Mechanoreceptors (respiratory muscles) Hypoxia (carotid and aortic bodies) Airflow (airway and parenchymal receptors) Changes in PCO2/pH (medullary center) Irritants (airway and parenchymal receptors) Medullary center (afferent input and efferent output) Cortical function (sense of effort)

10. Etiology The most common causes include Asthma Pneumonia COPD Myocardial ischemia Deconditioning The most common cause of dyspnea in patients with chronic pulmonary or cardiac disorders is Exacerbation of their disease

16. Approach to a Patient It is a subjective phenomenon, the perception of dyspnea and its interpretation vary from patient to patient Begin with a nonleading question: Do you have any difficulty breathing? If the response is affirmative and dyspnea is established as a problem, it should be characterized in detail. When did it begin? Has the onset been sudden or insidious? Inquire about the frequency and duration of attacks. The conditions in which dyspnea occurs should be ascertained Ask about associated symptoms: chest pain, palpitations, wheezing, or coughing

17. Sometimes a nonproductive cough may be present as a "dyspnea equivalent." What other significant medical problems does the patient have, and what medications has he been taking? How much has he smoked? Ask if he has noticed any recent or progressive limitation in his ability to conduct specific tasks that he was able to perform without difficulty in the past Additional questions should be aimed at ascertaining whether the patient has orthopnea or paroxysmal nocturnal dyspnea Inquire about the number of pillows he uses under his head at night and whether he has ever had to sleep sitting up.

18. Does he develop coughing or wheezing in the recumbent position? Did he ever wake up at night with shortness of breath? How long after lying down did the episode occur, and what did he do to relieve his distress? Characteristically, the patient with left ventricular failure sits up at bedside, dangles his feet, and refrains from ambulation or other activity that is likely to worsen his symptoms.

20. NHYA(NEW YORK HEART ASSOCIATION) DYSPNOEA SEVERITY SCALE · Grade IV: Dyspnea at rest. · Grade III: Dyspnea while doing day to day activities like bathing, changing    clothes etc. · Grade II: Dyspnea while doing regular and normal activity · Grade I: While doing more than normal activity.

21. DYSPNOEA INDEX The Dyspnea Index is one measure of shortness of breath for determining exertion levels. Level 0: No shortness of breath; can count to 15 (takes about 8 seconds) without taking a breath in the sequence. Level 1: Mild shortness of breath; can count to 15 but must take one short breath in the sequence. Level 2: Moderate shortness of breath; need to take 2 breaths to count to 15 in the sequence. Level 3: Definite shortness of breath; must take three breaths in the sequence of counting to 15. Reduce level of intensity and use breathing control techniques. Level 4: Severe shortness of breath; unable to count or speak. Cease activity immediately 

22. Standard of Care 1. Assessment 2. Diagnosis 3. Education 4. Treatment: Non-pharmacological 5. Treatment: Pharmacological 6. Crisis Intervention

23. Exam Nose and sinus examination Fluid status exam Jugular Venous Distention Hepatojugular Reflex Peripheral Edema Peripheral Vascular Exam Decreased pulses or bruits Respiratory Exam Increased AP Chest diameter Wheezing Rales Cyanosis Clubbing Accessory muscle use (Neck, chest, abdomen) Speaking in phrases to catch breath

24. Cardiac Auscultation Tachycardia S3 Gallup Rhythm Cardiac Murmur Psychomotor exam Anxiety

25. Easily Performed Diagnostic Tests Chest radiographs Electrocardiograph Screening spirometry

26. In cases where test results inconclusive complete PFTs ABGs EKG Standard exercise treadmill testing/ or complete cardiopulmonary exercise testing Consultation with pulmonologist/cardiologist may be useful

27. ABGs Commonly used to evaluate acute dyspnea can provide information about altered pH, hypercapnia, hypocapnia or hypoxemia normal ABGs do not exclude cardiac/pulmonary dx as cause of dyspnea Remember- ABGs may be normal even in cases of acute dyspnea - ABGs do not evaluate breathing

28. PULSE OX Rapid, widely available, noninvasive means of assessment in most clinical situations- insensitive (may be normal in acute dyspnea) The % of Oxygen saturation does not always correspond to PaO2 The hemoglobin desaturation curve can be shifted depending on the pH, temperature or arterial carbon monoxide or carbon dioxide levels

29. Diagnostic Interventions Think back to the differential: PULMONARY VS. EXTRAPULMONARY CXR? is it the lungs? ECG? is it the heart? ABG? what is the imbalance? LABS?r/o other causes.

30. CAUSES OF DYSPNOEA WITH NORMAL X-RAY Airways disease (asthma, upper airways obstruction, bronchiolitis) Pulmonary vascular disease (pulmonary embolism, primary pulmonary hypertension, intrapulmonary shunt) Early parenchymal disease (e.g. sarcoid, interstitial pneumonias, infection(viral, PCP) Cardiac disease (e.g. angina, arrhythmia, valvular disease, intracardiac shunt) Neuromuscular weakness Metabolic acidosis Anaemia Thyrotoxicosis Hyperventilation syndrome

31. Distinguishing cardiac & respiratory causes of dyspnoea This can be difficult. Resting ECG is useful in practice, a cardiac cause of breathlessness is unlikely in the setting of a completely normal ECG. Exercise ECG, echo, and cardiac catheterization may be required. Measurement of B-type natriuretic peptide (BNP) is a recent development that may be of value in the diagnosis of cardiac failure; in patients presenting as an emergency with breathlessness, a serum BNP level <50 ng/l makes cardiac failure very unlikely. Cardiac and respiratory diseases can of course coexist.

32. DYSPNOEA DIFFERENTIAL INDEX Dyspnea differential index = PEFR × PaO2 /1000 PEFR decreased in respiratory disease <200-respiratory cause >200-cardiac cause

33. Dyspnea equivalent .  Many times angina is worst during moments of exertion. This is because the demand for oxygenated blood increases when heart rate increases. If the coronary arty is narrowed then it will have difficulty supplying the blood as fast as the heart needs it. The result is angina or in some cases dyspnea equivalent angina. The only way to relieve the angina is through resting to bring the heart rate back to normal and lower the demands for oxygenated blood

34. Treatment

36. Treatment: Non-pharmacological Energy conservation and breath control • Explain how to incorporate pacing and planning. • Teach relaxation training and breath control. • Encourage activity to tolerance and assist with energy conservation. Refer to Occupational Therapy (OT) – for energy conservation, Physiotherapy (PT) – for breath control for consultation when patient situations are highly complex. Air flow • Open windows and air movement, such as a fan, can be very helpful. Cool air blowing on the face likely triggers reflexes in trigeminal nerve, providing a sense of relief from dyspnea. Environment • Cool and humidify dry air, eliminate irritants in air. Maintain loose sheets over the patients and ensure visitors are not “crowding” the patient.

37. Positioning • Avoid compression of abdomen or chest when positioning. • Try placing in semi-Fowlers position (raising head and upper torso). • Patient may direct optimal position for him/her self Support • Offer psychosocial support and/or counseling. • Alternative therapies for relaxation include: massage, therapeutic touch, visualization, music therapies. • Acupuncture or acupressure

39. Underlying causes of dyspnoea & treatment of choice

43. Oxygen • There are multiple triggers contributing to the sensation of dyspnea. Hypoxemia is only one. Measure oxygen saturation to determine if hypoxemia is a factor in the patient’s experience of dyspnea. • Careful selection is necessary to identify those people who will benefit from oxygen therapy. Individualized care is paramount. Hypoxic patients: • There is low-grade scientific evidence that both oxygen and airflow improve dyspnea in hypoxic patients with advanced disease at rest. • Provide supplemental oxygen therapy for hypoxic patients according to the Home Oxygen Program guidelines . Non-hypoxic patients: • A systematic review showed that there is insufficient evidence that supplemental oxygen is beneficial for non-hypoxic patients. • Use other interventions as first line to manage dyspnea with non-hypoxic patients. • The Home Oxygen Program guidelines will not fund supplemental oxygen at home for non-hypoxic patients. • If dyspnea is not managed with maximum treatment and medications, refer for a Hospice Palliative consultation, if available.

44. Education Dyspnea is a distressing symptom to experience and to witness. Providing information and education is foundational to enhance the patient and family’s ability to cope Explain to the patient and family what is understood about the multiple triggers of dyspnea (i.e., restriction of respiratory movement, obstructions, and muscle weakness). It is not simply related to oxygenation and therefore many different strategies together can make a difference. Reinforce that this is a symptom that can be managed. Develop a clear plan for the patient and family to address the pattern of shortness of breath and the patient’s way of coping.

45. Teach the purpose of each medication, particularly opioids, as families often do not understand the role of these medications. Ensure an understanding of using regular and breakthrough medications. This is a key to effective management. • Known COPD patients often use inhalers incorrectly. Consider the use of nebulizers and spacers. Ensure patient’s compliance. • Review Shortness of Breath teaching pamphlet with patient and family

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