The lungs are fully inflated within the cavity because the pressure inside the airways (intrapulmonary pressure) is higher than the pressure inside the pleural space (intrapleural pressure). Despite the low pressure in the pleural space, air does not enter it because there are no natural connections to an air-containing passage, and the pressure of gases in the bloodstream is too low for them to be forced into the pleural space. Therefore, a pneumothorax can only develop if air is allowed to enter, through damage to the chest wall or damage to the lung itself, or occasionally because microorganisms in the pleural space produce gas. Once air enters the pleural cavity, the intrapleural pressure increases resulting in the difference between the intrapulmonary pressure and the intrapleural pressure (defined as the transpulmonary pressure) to equal zero which cause the lungs to deflate in contrast to a normal transpulmonary pressure of ~4 mm Hg.Chest-wall defects are usually evident in cases of injury to the chest wall, such as stab or bullet wounds ("open pneumothorax"). In secondary spontaneous pneumothoraces, vulnerabilities in the lung tissue are caused by a variety of disease processes, particularly by rupturing of bullae (large air-containing lesions) in cases of severe emphysema. Areas of necrosis (tissue death) may precipitate episodes of pneumothorax, although the exact mechanism is unclear.
A diagnosis of inappropriate sinus tachycardia is primarily one of exclusion, and the following may be observed:
Exclusion of all other causes of sinus tachycardia
Common forms of supraventricular tachycardia (SVT) must be excluded
Normal P wave morphology
A resting sinus tachycardia is usually (but not always) present
Nocturnal dip in heart rate
Inappropriate heart rate response on exertion
Mean heart rate in 24hrs >95 bpm
Symptoms are documented to be due to tachycardia
Hypotension is occasionally observed
Syncope (fainting) is occasionally reported

Treatment
IST has been treated both pharmacologically and invasively, with varying degrees of success. IST, in and of itself, is not indicative of higher rates of mortality, and non-treatment is an option chosen by many if they have minimal symptoms.Some types of medication tried by cardiologists and other physicians include: beta blockers, selective sinus node If channel inhibitors (such as ivabradine), calcium channel blockers, and antiarrhythmic agents. Some SSRI drugs are also occasionally tried, as are treatments more commonly used to treat postural orthostatic tachycardia syndrome, such as fludrocortisone.Invasive treatments include forms of catheter ablation such as sinus node modification (selective ablation of the sinus node), complete sinus node ablation (with associated implantation of a permanent artificial pacemaker), and AV node ablation in very resistant cases (creation of iatrogenic complete heart block, necessitating implantation of a permanent artificial pacemaker). However, invasive treatments can also make the symptoms worse. See also
Supraventricular tachycardia
Sinus tachycardia
Postural orthostatic tachycardia syndrome
Dysautonomia

References
Further reading
Yusuf, Shamil; Camm, A. John (2005). "Deciphering the sinus tachycardias". Clinical Cardiology. 28 (6): 267–76. doi:10.1002/clc.4960280603. PMC 6654702. PMID 16028460. Still, A; Raatikainen, P;  et al. (2005).