Aetiology of OSA

Snoring is a result of incomplete pharyngeal obstruction.

Turbulent airflow and subsequent progressive vibratory trauma to the soft tissues of the upper airway are important factors that contribute to the condition.

Anatomic obstruction leads to increased negative inspiratory pressure, which propagates further airway collapse, turbulence, and noise.

The imbalance between the forces that act to maintain airway patency (the force of the pharyngeal muscles) and the negative inspiratory forces generated by the diaphragm is thought to be the primary etiology of anatomic obstruction in OSA.

In OSA, the tongue contacts the soft palate and posterior pharyngeal wall in the presence of lateral collapse of the pharynx, generating occlusion.

Significant factors that contribute to this condition include

• obesity
  
• redundant tissue in the neck
• retrognathia
  
• craniofacial anomalies
  
• anatomic abnormalities of the nasal airway (eg, septal deviation, inferior turbinate hypertrophy, nasal-valve narrowing, adenoid hypertrophy)
  
• Alcohol and other sedatives may increase the severity of OSA.
  
• Data from a recent meta-analysis by Rada also suggested a causal relationship between OSA and head and neck cancer (which may first manifest as OSA).

In children :

OSA in children is usually due to large tonsils and adenoids. There is no relation, however, between tonsils and adenoid size and the degree of OSA. This is probably due to the combined effects of muscle tone, pharyngeal size and adenotonsillar hypertrophy.

High risk groups include children with craniofacial anomalies, cerebral palsy, muscular dystrophy and Down syndrome.
Children with OSA are not usually obese, but OSA does occur frequently in morbidly obese children and adolescents.

Source : The American Sleep Apnea Association (ASAA)

Pathophysiology and Aetiology

Aetiology and Pathophysiology of Hypertension- Arterial pressure is determined by the cardiac output (systolic) and the resistance (diastolic) in the vessels and is regulated by the Renin Angiotensin-Aldosterone System
- Peripheral vascular resistance is dependent on vessel structure and function, especially arterioles.
It is important to realize that there are two types of hypertension, essential (cause is unknown) or secondary (from an underlying disorder such as renal disorder).

Primary (Essential) Hypertension
Thought to be caused or at least influenced by weight gain and a sedentary lifestyle.
-Cardiac output is increased due to the additional blood flow needed for adipose tissue and the increased metabolic demands of the heart, gastro-intestinal tract, kidneys and muscle. This increases total peripheral resistance as well, for tissues that do not require the extra blood which then results in local regulation and vasoconstriction.

-Increased sympathetic activity, especially in the kidneys. This is not well understood but thought to be due to leptin (a hormone released from adipose cells), which may stimulate multiple regions of the hypothalamus and has an excitatory effect on the vasomotor center in the medulla.

-Angiotensin II and aldosterone levels increased mostly due to the increased sympathetic stimulation which leads to increased renin release, which means elevated levels of angiotensin II which then stimulates the adrenal gland to secrete more aldosterone (which increases reabsorption of salt and water). This increases extracellular volume which will lead to increased blood volume, venous return and cardiac output.

-Renal pressure natriuresis mechanism is impaired and kidneys will not excrete salt and water unless the arterial blood pressure is high, that is, if blood pressure artificially reduced to normal blood pressure levels, there will be no excretion of salt.

Secondary Hypertension
This is due to underlying disorders, such as renal disease, adrenal tumours (excessive aldosterone secreted) or a renal artery stenosis.