This document discusses breathlessness (dyspnea) and tachycardia. It defines breathlessness and describes scales to assess severity. Positional breathlessness is discussed. Causes of acute, subacute and chronic dyspnea are provided. Tachycardia is evaluated based on ECG findings of QRS duration and rhythm regularity. Common adult tachycardias like sinus tachycardia, atrial fibrillation, atrial flutter, SVT are summarized. Management of various tachycardias is outlined.

1. Breathlessness and Tachycardia
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.

3. Classification
• 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. Positional breathlessness:
• Orthopnoea 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.
• 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 SOB 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.

5. 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

6. Etiology
Dyspnea has many pulmonary, cardiac, and other causes which vary by acuity of onset :
• Some Causes of Acute* Dyspnea,
• Some Causes of Subacute* Dyspnea,
• Some Causes of Chronic* Dyspnea).
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).

7. 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.

8. 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.

9. 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.

10. Dysfunction Breathing
• Sensation of inability to inflate lungs fully.
• Feeling of the need to take deep breaths or sigh.
• Breathlessness varies with social situation.
• Breathlessness when talking but not on exercise.
• Very variable exercise tolerance.
• Dizziness.
• Tingling in the fingers or around the mouth.
• Symptoms reproduced by Taking 20 deep breaths in the clinic.
• Previous “Somatisation” disorders.

11. Some Causes of Acute Dyspnea

12. Some Causes of Acute Dyspnea

13. Some Causes of Acute Dyspnea

14. Some Causes of Acute Dyspnea

15. Some Causes of Sub Acute Dyspnea

16. Some Causes of Sub Acute Dyspnea

17. Some Causes of Chronic Dyspnea

18. Some Causes of Chronic Dyspnea

19. Some Causes of Chronic Dyspnea

20. 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

21. 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.

22. 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.

23. 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.

24. Tachycardia
• A rapid heart rate or tachycardia while at rest is usually evidence of a
problem, but the tachycardia may not be the problem.
• The evaluation of tachycardias (heart rate >100 beats/min) is based
on 3 ECG findings: i.e., the duration of the QRS complex, the
uniformity of the R-R intervals, and the characteristics of the atrial
activity.
• The duration of the QRS complex is used to distinguish narrow-QRS-
complex tachycardias (QRS duration ″0.12 sec) from wide-QRS-
complex tachycardias (QRS duration >0.12 sec) This helps to identify
the point of origin of the tachycardia

25. Flow Diagram for the evaluation of Tachycardia

26. Adult tachycardia with a Pulse Algorithm

27. Normal Sinus Rhythm (NSR)

28. Sinus Tachycardia

29. Atrial Arrhythmias

30. Atrial Arrhythmias

31. Atrial Fibrillation (AF)

32. Atrial Fibrillation (AF)

33. Atrial Fibrillation (AF)

34. Atria Flutter (Afl)

35. Atrial flutter: Management
Treatment options for Aflutter include the following:-
1. DC Cardioversion-Synchronised 100 Joules
2. Antiarrhythmic drugs/nodal rate control agents like CCB-Diltiazem,
Betablocker-Esmolol, Cardiac Glycosides-Digoxin, others-
Amiodarone,propafenone,sotalol,procainamide,disopyramide,ibutili
de,flecainide.
3. Rapid atrial pacing to terminate atrial flutter
4. Antithrombotic therapy same as in AF

36. PSVT

37. PSVT Inj. Adenosin

38. SVT

39. Torsade de Pointes

40. Ventricular Fibrillation (VF)

41. Ventricular Tachycardia (VT): Monomorphic

42. Wide QRS complex tachycardia:Management

43. Ventricular(VT): Polymorphic

44. VT: Polymorphic Management
The management of polymorphic VT is summarised as follows:
1. Sustained polymorphic VT requires non synchronised electro cardio-
version (i.e. defribrillation)
2. For torsade de pointes, I.V. Mg is used for pharmacological MM (and can
be combined with electrical cardioversion). There is no universal dosing
for Mg. ACLS guidelines recommend 1-2 gm MgSO4 IV over 15 mts.
While another recommended regimen is 2 gm MgSO4 as an IV bolus f/by
continuous infusion 2-4 mg/min.
3. Correcting high risk electrolyte abnormalities and high risk drugs to
prevent recurrence.
4. For polymorphic VT with Normal QT interval amiodarone or beta blocker
(for myocardial ischaemia) can help to prevent recurrences.

45. THANK YOU