Tamaka shwas exacerbarates with shita whereas shita is treatment for pratamaka shwas. Chakrapani has given 2 reasoning for the same. Pittanubanda in pratamaka pacifies by shita treatment or as in madatyaya wherein madyapana is treatment of mada which is caused by excessive alcoholic intake, similarly shita chikitsa by its viparitharthakari chikitsa helps in pratamka condition of tamaka shwas. Features of Pratamaka and Santamaka Shvasa resembles exacerbations. Vata and kapha when associated with pitta lead to pratamaka wherein fever is the main symptom which explains the presence of pitta. Infection is main cause of exacerbation which leads to secretion of inflammatory factors which may stimulate prostaglandins and thereby fever cascade. Studies suggest that acquiring a new strain of bacteria is associated with increased near-term risk of exacerbation and that bacterial infection/superinfection is involved in over 50% of exacerbations. Viral respiratory infections are

d īrghaṁ śvasiti means Prolonged expiration which is observed in following diseases  Asthma, Bronchietasis, Bronchitis, Collapse, COPD, Emphysema, Epiglottitis, Fibrosis, Foreign body, Good Pasture syndrome, Lung cancer, Meconium aspiration syndrome, Pneumoconiosis, Pneumonia, Pneumonia, eosinophilic, Rostan asthma, Sarcoidosis, Tuberculosis. Airflow limitation during the expiratory phase in airway obstructive disease (ślēṣma āvr̥ta mukhasrōtāḥ) causes prolonged expiration, which is one of the hallmarks of COPD.  Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD)

Charakokta mahāshvāsa  dūrādvijñāyatē bhr̥śam:  breathing sound is such that it can be heard from distance. Stridor (Latin for "creaking or grating noise") is a high-pitched breath sound resulting from turbulent air flow in the larynx or lower in the bronchial tree. Stridor is a physical sign which is caused by a narrowed or obstructed airway. It can be inspiratory, expiratory or biphasic, although it is usually heard during inspiration. Inspiratory stridor often occurs in children with croup. It may be indicative of serious airway  obstruction  from severe conditions such as epiglottitis, a foreign body lodged in the airway, or a laryngeal tumor. Stridor should always command attention to establish its cause. ( https://en.wikipedia. org/wiki/Stridor ) mattarṣabha ivāniśa:  explains the nasal flares. Nasal flaring  is when the nostrils widen while a person is breathing. It is a sign that the person is having difficulty breathing. It is most commo

प्रतिलोमं यदा वायु स्रोतांसि प्रतिपद्यते ! ग्रीवां शिरश्च संग्रह्य श्लेष्माणं समुदीर्य च !! (Ch. Chi.-17 / 55 ) Charakokta Tamaka shvaasa  pratilōmaṁ yadā vāyu i.e. normal gati of vata is hampered. A specific movement of gases takes place in the alveoli from high pressure to low pressure. Oxygen moves from alveoli into blood whereas CO2 moves from blood to alveoli from where it is expired out. This movement of gases is coordinated normally by vata but when its channels are obstructed by either excessive secretion or reduced absorption of kapha (mucus), vata gets vitiated and exchange of gases does not takes place. The symptoms are presented firstly with upper respiratory tract involvement. Pinasa is the prior symptoms followed by wheezing sound (ghurghurukaṁ). The presentation explains allergic diasthesis.  Allergic rhinitis is prodormal symptom in EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS (EGPA).  करोति पीनसं तेन रूद्धो घुर्घुरकं तथा ! अतीव तीव्रवेगं च श्वासं प

मारुतः प्रणवाहीनि स्रोतांसि आविश्य  कुप्यति ! उरस्थ: कफमुद्धूय हिक्काश्वासाङकरोति  !!                                                   (Ch.chi.17/17)   Explains the hyperplasia of mucus secretion as seen in COPD wherein small airways may become narrowed by cells (hyperplasia and accumulation), mucus, and fibrosis. Characteristic cellular changes include goblet cell metaplasia, with these mucus-secreting cells replacing surfactant-secreting Clara cells. Smooth-muscle hypertrophy (kupyati maruta) may also be present.  These abnormalities may cause luminal narrowing by fibrosis, excess mucus, edema, and cellular infiltration. Vitiated vata expels kapha from its sthana can be easily understood in case of cystic fibrosis. Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) which is an integral membrane protein that functions as an epithelial anion channel. The ~1480-amino-acid molecule encodes a passive conduit for chloride and bicarbonate transport across plasma membrane

रजसा धूमवाताभ्यां शीतास्थानाम्बुसेवनात् ! व्यायामाद्-ग्राम्यधर्म-अध्व-रूक्षान्न-विशमाशनात् !! आमप्रदोषात्-आनाहाद्रौक्ष्यादत्यपतर्पणात् ! दौर्बल्यात् मर्मणोघाताद् द्वन्द्वात् शुद्धि-अतियोगात्!! अतिसार-ज्वर-च्छर्दि-प्रतिश्याय-क्षत-क्षयात् ! रक्तपित्तादुदावर्ताद्-विसूच्यलसकादपि !!        (Ch.Chi.17/10-16) Asthma is a heterogeneous disease with interplay between genetic and environmental factors. Several risk factors that predispose to asthma have been identified. These should be distinguished from triggers, which are environmental factors that worsen asthma in a patient with established disease. Diet- The role of dietary factors is controversial. Observational studies have shown that diets low in antioxidants such as vitamin C and vitamin A, magnesium, selenium, and omega-3 polyunsaturated fats (fish oil) or high in sodium and omega-6 polyunsaturated fats are associated with an increased risk of asthma. Vitamin D deficiency may also predispose to the development of asthma