The muscles of the face are usually spared, but in rare cases, the eye muscles may be weakened, leading to ophthalmoplegia.Respiratory difficulties can be caused by atrophy of the muscles between the ribs (intercostals), atrophy of the diaphragm muscle, and degeneration of the nerve that stimulates the diaphragm (phrenic nerve). This can prolong the time it takes to wean a person off of a breathing machine (mechanical ventilation) by as much as 7 – 13 days.Deep tendon reflexes may be lost or diminished, and there may be bilateral symmetric flaccid paralysis of the arms and legs. The nervous system manifestations are typically limited to peripheral nerves, as the central nervous system is usually unaffected. Cause
The causes of CIP and CIM are unknown, though they are thought to be a possible neurological manifestation of systemic inflammatory response syndrome. Pathology
Nerve biopsy would show axonal neuropathy, but it is no longer indicated. A muscle biopsy of critical illness myopathy would show selective loss of thick filaments in muscle, demonstrating the loss of myosin and the presence of muscle cell death (necrosis). When muscles lose stimulation from neurons, they can undergo degeneration. However, when critical illness myopathy occurs, it is not solely due to loss of innervation of the muscle. With critical illness myopathy, no other cause of the muscle degeneration can be found.Unlike Guillain Barre Syndrome, another neurological disorder that causes weakness, patients with critical illness polyneuropathy do not have loss of the myelin sheath that normally surrounds neurons (demyelination).
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).