Approach a patient of Dyspnea in critical area

1. Approach to patient of Dyspnea
By
Dr. Rakesh K. Solanki

2. Definition
• Dyspnea is unpleasant or uncomfortable breathing. It is experienced and described
differently by patients depending on the cause.
• Breathlessness is the end result of complex signalling involving lungs, thorax, heart,
and skeletal muscles, as well as the inputs and outputs of various CNS sites.
Prognostically and diagnostically it is a poor discriminator.
• Subjective experience of breathing discomfort that consists of qualititatively distict
sensations that vary in intensity. The experience derives from interactions among
multiple physiological, physchological, social, and environmental factors and may
induce secondary physiological and behavioural responses.
(Am J Respir Crit Care Med 1999; 159:321-40)

3. Classification – modified Medical Research
Council (MRC)
• There are a number of simple scales to assess the severity of breathlessness - eg, the
modified Medical Research Council (MRC) dyspnoea score:
• Grade 0: not troubled by breathlessness except on strenuous exertion.
• Grade 1: short of breath when hurrying on level ground or walking up a slight incline.
• Grade 2: walks slower than contemporaries because of breathlessness, or has to stop for
breath when walking at own pace.
• Grade 3: stops for breath after walking about 100 metres or stops after a few minutes of
walking on level ground.
• Grade 4: too breathless to leave the house or breathless on dressing or undressing.
NB: there is no accepted gold standard for measuring breathlessness - unidimensional tools
such as the above are recommended for assessing severity but multidimensional tools are
required to capture the impact on quality of life[8].

4. Classification - NYHA
NYHA Classification
• Class I - No symptoms and no limitation in ordinary physical activity, e.g. shortness
of breath when walking, climbing stairs etc.
• Class II - Mild symptoms (mild shortness of breath and/or angina) and slight
limitation during ordinary activity.
• Class III - Marked limitation in activity due to symptoms, even during less-than-
ordinary activity, e.g. walking short distances (20-100m–).Comfortable only at rest.
• Class IV - Severe limitations. Experiences symptoms even while at rest. Mostly
bedbound patients.

5. Classification – VISUAL ANALOG SCORE

6. Receptors involved in mechanism of Dyspnea
• 1. J Receptors – Alveolo-capillary junction
• Stimualated by pulmonary congestion, oedema and microemboli.
• Responsible for rapid shallow breathing
• 2. Stretch receptors – Thorasic cage and lung
• 3. Chemoreceptors – Carotid arteries, aorta and reticular substance of medulla
• Stimulated by hypoxia, excess of CO2 and decrease in pH.
• 4. Receptors in the respiratory muscle – Immediate cause of appreciation of
Dysnoea.

7. Mechanism of Dyspnea

9. Schematic representation of afferent pathways from respiratory muscle mechanoreceptors to the CNS. DRG = dorsal respiratory
group; VRG = ventral respiratory group.

10. Schematic representation of afferent pathways of dyspnea from vagal receptors and peripheral chemoreceptors to the CNS. The
precise pathways from the nucleus tractus solitarius to the limbic system and cortex are not clearly delineated and, hence, are shown as
broken lines. RAR = rapidly adapting receptor; SAR = slowly adapting receptor.

11. Positional breathlessness:
• Orthopnoea is dyspnea on lying down position typifies cardiogenic pulmonary oedema, but may also be
seen in diaphragmatic weakness and severe COPD.
• Most Patient with Breathlessness not just those with Heart Failure feels worse when they lie down
• Patients with expiratory muscle weakness (e.g. myotonic dystrophy may prefer to lie flat.)
• Orthodeoxia (desaturation on sitting up) is associated with the intrapulmonary shunting seen in
hepatopulmonary syndrome.
• Paroxysmal Nocturnal dysnoea is Choking and gasping episodes awakening patient from sleep (separate
from orthopnoea) suggest sleep-related upper airway obstruction, which is a potential ‘accelerating’ factor
for both pulmonary arterial hypertension and hypoventilatory respiratory failure.
• Platypnoea is dyspnoea on upright posture seen in Intra-Cardiac Shunt (ASD), AV Malformations, Cirrhosis
with pulmonary spider naevi, Lung Disease predominantly affecting lower lobes, Supraglottic tumour,
Autonomic Failure.
• Trepopnea is dyspnoea on lateral recumbent postion seen in Chronic CHF, diseases affecting one Major
Bronchus.

13. Sudden Onset Vs Gradual Onset:
• Sudden Onset is seen in Pulmonary Emboli, Pneumothorax, Left ventricular Failure,
Inhalational of a Foreign Body and Asthma.
• Gradual Onset suggests Fibrotic Lung Disease, Pleural Effusion, Anaemia or Lung
Cancer.
THINK ABOUT POSSIBILITY OF PULMONARY EMBOLISM EVERY
TIME WHEN YOU SEE PATIENT WHO IS BREATHLESS

14. History
• History of present illness should cover the duration, temporal onset (eg, abrupt,
insidious), and provoking or exacerbating factors (eg, allergen exposure, cold, exertion,
supine position). Severity can be determined by assessing the activity level required to cause
dyspnea. Physicians should note how much dyspnea has changed from the patient’s usual
state.
• Past medical history should cover disorders known to cause dyspnea, including asthma,
COPD, and heart disease, as well as risk factors for the different etiologies: Smoking
history—for cancer, COPD, and heart disease
• Family history, hypertension, and high cholesterol levels—for coronary artery disease
• Recent immobilization or surgery, recent long-distance travel, cancer or risk factors for or
signs of occult cancer, prior or family history of clotting, pregnancy, oral contraceptive use,
calf pain, leg swelling, and known deep venous thrombosis—for pulmonary embolism
• Occupational exposures (eg, gases, smoke, asbestos) should be investigated.

15. Physical Examination
Vital signs are reviewed for fever, tachycardia, and tachypnea.
Examination focuses on the cardiovascular and pulmonary systems.
A full lung examination is done, particularly including adequacy of air entry and exit,
symmetry of breath sounds, and presence of crackles, rhonchi, stridor, and wheezing.
Signs of consolidation (eg, egophony, dullness to percussion) should be sought.
The cervical, supraclavicular, and inguinal areas should be inspected and palpated for
lymphadenopathy.
Neck veins should be inspected for distention, and the legs and presacral area should be
palpated for pitting edema (both suggesting heart failure).
Heart sounds should be auscultated with notation of any extra heart sounds, muffled heart
sounds, or murmur.
Conjunctiva should be examined for pallor. Rectal examination and stool guaiac testing
should be done.

16. Physical Examination
In Hyperventilation, the ECG can be abnormal with widespread T-wave inversion
and ST segment depression.
Patients often hyperventilate transiently when they are having an ABG sample taken.
You can only confidently diagnose breathing if there is a chronic respiratory
alkalosis, with a bicarbonate concentration of <20 mmol/litre.

17. Physical Examination
• Hypotension, Tachycrdia, Tachypnoea : Acute Pulmory Oedema & ARDS
• Hypertension in Dyspnoic patients : Hypertension related Disatolic Heart failure with
Pulmonary Oedema, Heart Failure, or Pheochormocytoma
• Pulsus Paradoxus : Asthama, COPD and Cardia Tamponade
• Elevated Neck Veins, Extra Heart Sounds (S3 Gallop Rhythm) and Fluid Retension :
Congestive Heart Failure
• Elevated Neck Veins, Pulsus Paradoxus, a pericardial knock, pericardial rub, and the
Kussumal’s sign : Constrictive Percarditis and Effusion
• Irregular or fast heart beat : Tachyrrhthmia or Atrial Fibrillation
• Loud S2 : Pulmonary Hypertension
• Systolic Murmur : Acute valvular insufficiency, Machanical valve malfucntion

18. Physical Examination
• Pursed Lip Breathing : COPD
• A Barrel Chest : Emphysema and Cystic Fibrosis
• Stridor : Upper airway obstruction
• Systolic Murmur : Acute valvular insufficiency, Machanical valve malfunction
• Hoarsenes : Laryngitis, Laryngeal Cord Tumour, Vocal Cord Palsy
• Trachea may deviate to away from lesion : Pneumothorax or large pleural effusion
• Unilateral Dullness to percussion : Pleural effusion, Atelectasis, FB Aspiration, Pleural
Tumour, Pneumonia
• Hyperresonance : Pneumothorax or severe Emphysema
• Sub cutaneous Emphysema : Pneumo mediastinum
• Cranial Nerve Palsy a/w dysnoea : Botulism
• Ptosis : Myasthenia Gravis, Myotonic Dystrophy, Botulism

19. Etiology
Dyspnea has many pulmonary, cardiac, and other causes which vary by acuity of onset :
• Some Causes of Acute* Dyspnea, (acute occurs within minutes of triggering events)
• Some Causes of Subacute* Dyspnea, (subacute occurs with hours or days)
• Some Causes of Chronic* Dyspnea). (lasted for weeks to years)
The most common causes include
• Asthma
• Pneumonia
• COPD
• Myocardial ischemia
• Physical deconditioning
The most common cause of dyspnea in patients with chronic pulmonary or cardiac disorders is
Exacerbation of their disease
However, such patients may also acutely develop another condition (eg, a patient with long-standing
asthma may have a myocardial infarction, a patient with chronic heart failure may develop pneumonia).

20. Some Causes of Acute Dyspnea

21. Some Causes of Acute Dyspnea

22. Some Causes of Sub Acute Dyspnea

23. Some Causes of Chronic Dyspnea

24. Some Causes of Chronic Dyspnea

25. Some Causes of Chronic Dyspnea

26. Red flags
The following findings are of particular concern:
Dyspnea at rest during examination
Decreased level of consciousness or agitation or confusion
Accessory muscle use and poor air excursion
Chest pain
Crackles
Weight loss
Night sweats
Palpitations

27. Testing
Pulse oximetry should be done in all patients, and a chest x-ray should be done as well unless
symptoms are clearly caused by a mild or moderate exacerbation of a known condition.
Most adults should have an ECG to detect myocardial ischemia (and serum cardiac marker testing if
suspicion is high) unless myocardial ischemia can be excluded clinically.
In patients with severe or deteriorating respiratory status, ABGs should be measured to more
precisely quantify hypoxemia, measure Paco2, diagnose any acid-base disorders stimulating
hyperventilation, and calculate the alveolar-arterial gradient.
Patients who have no clear diagnosis after chest x-ray and ECG and are at moderate or high risk of
having pulmonary embolism (from a clinical prediction rule) should undergo CT angiography or
ventilation/perfusion scanning. Patients who are at low risk may have d-dimer testing (a normal d-
dimer level effectively rules out pulmonary embolism in a low-risk patient).
Chronic dyspnea may warrant additional tests, such as CT, pulmonary function tests,
echocardiography, and bronchoscopy
CBC, RFT, LFT, Thyroid Function Test, ESR, 2 D ECHO, Spirometry etc.

28. Testing

29. Dyspnea in COVID19 patients
• Multiorgan involvement i.e. lungs, heart, kidney, GIT & coagulation system but
Respiratory System is the most commonly engaged organ.
• It may lead to ARDS especially to elderly and with co-morbid conditions.
• It is associated with significant Dyspnea, it imposes hypoxia that could be due to
high shunt physiology i.e hypoventilated areas of lungs are hyperemic.
• Onset of dyspnea particularly with precipitous drops in Oxygen saturation especially
with exertion can help clinicians to more easily distinguish COVID19 from others.

30. Dyspnea in COVID19 patients
• One relevant feature of the Covid‐19 disease is the absence of dyspnea, described as
‘shortness of breath’ or ‘an unpleasant urge to breathe’. The lack of dyspnea is
observed even in the most severe cases, in which subjects present tachypnea and
tachycardia. In the Wuhan cohort, 62.4% of severe cases and 46.3% of those who
ended up intubated, ventilated or dead did not present dyspnea [1, 2.
• The afferent fibers that appear to play the most relevant role in dyspnea are the
pulmonary C‐fibers, which are predominantly located below the alveolar membrane.
• Although local changes in viral pneumonia could stimulate C‐pulmonary fibers, the
cytokine storm syndrome (which is rather characteristic of Covid‐19) could damage
these neurons and therefore explain a total or partial loss of their function. However,
this hypothesis collides with the fact that some viral respiratory infections induce an
upregulation of receptors from these afferent sensory fibers [4.

31. Treatment
• Best treatment is correction of the underlying disorder.
• Hypoxemia is treated with supplemental oxygen as needed to maintain oxygen saturation >
88% or PaO2> 55 mm Hg because levels above these thresholds provide adequate oxygen
delivery to tissues. Levels below these thresholds are on the steep portion of the oxygen–Hb
dissociation curve, where even a small decline in arterial oxygen tension can result in a large
decline in Hb saturation.
• Oxygen saturation should be maintained at > 93% if myocardial or cerebral ischemia is a
concern, although recent data suggest that supplemental oxygen is not beneficial in the
treatment of acute myocardial infarction unless the patient has hypoxia.
• Morphine 0.5 to 5 mg IV helps reduce anxiety and the discomfort of dyspnea in various
conditions, including myocardial infarction, pulmonary embolism, and the dyspnea that
commonly accompanies terminal illness. However, opioids can be deleterious in patients
with acute airflow limitation (eg, asthma, COPD) because they suppress the ventilatory drive
and can worsen respiratory acidemia.

32. Treatment
• Treat the underlying cause
• 1. Pneumothorax : Closed tube thoracostomy
• 2. FB Removal
• 3. Asthma : Bronchodilators, Steroids
• 4. Anaphylaxis : Adrenaline and avoidance of precipitating agents

33. Key Points
• Pulse oximetry is a key component of the examination.
• Low oxygen saturation (< 90%) indicates a serious problem, but normal
saturation does not rule one out.
• Accessory muscle use, a sudden decrease in oxygen saturation, or a decreased
level of consciousness requires emergency evaluation and hospitalization.
• Myocardial ischemia and pulmonary embolism are relatively common, but
symptoms and signs can be nonspecific.
• Exacerbation of known conditions (eg, asthma, COPD, heart failure)
is common, but patients may also develop new problems.

34. Reference
• www.medscape.com
• www.msdmanual.com/professional
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2972628/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7177114/
• www.chestpubs.org
• Mechanism of Dyspnea by Nausherwan K Burki
• European Journal of Neurology
• Infectious disease advisor
• Slideshare.net

35. THANK YOU