Since my primary physiologic concern during cosmetic rhinoplasty centers on the breathing function and the nasal valve is the most critical area for breathing, a review of both the anatomy and physiology of the nasal valve area is imperative. Regarding the anatomy, an arbitrary subdivision of the nasal valve for practical clinical thinking has been forwarded in the literature, suggesting that we think of the nasal valve area as having two component parts. First, the internal nasal valve (most of our discussion will center around the internal nasal valve as it is composed of a number of diverse anatomic parts) and an external nasal valve, which is primarily composed of the lower lateral cartilages and surrounding soft tissues, which are covered both dorsally and ventrally by skin. Both valves (internal and external) are still subjected to the laws of fluid (air is the fluid) dynamics (Barelli et al. 1987; Bridger 1970; Bridger and Proctor 1970; Cole 2000, 2003; de Wit et al. 1965; Eccles 2000; Haight and Cole 1983; Hilberg et al. 1989; Hinderer 1971; Huizing and de Groot 2003; Kasperbauer and Kern 1987; O’Neill and Tolley 1988; Van Dishoeck 1942, 1965; Wexler and Davidson 2004).

Today, 40 years after Williams merely speculated that the nasal valve functions as a type of inflow device controlling the rate and depth of respiration, the complete function of the nasal valve is still unknown (Williams 1972). Hinderer suggested that the nasal valve controls inspiratory air currents changing them from a column to a sheet of air, thereby giving shape, velocity, direction, and resistance to the inspired air (Hinderer 1970, 1971). It has been previously suggested that the head of the inferior turbinate (Gray 1970) and the septal turbinate (Barelli et al. 1987; Cottle et al. 1958; Wexler and Davidson 2004) work in concert and both are important components of the internal nasal valve area because they provide the necessary resistance to breathing during inspiration. The nasal valve has been considered (Bridger 1970; Bridger and Proctor 1970) to function as a Starling resistor influenced by Bernoulli forces so that when the airflow increases (accelerates), the interior nasal pressure decreases allowing the lateral nasal walls to collapse inward (towards the nasal septum). Both the nose and a Starling resistor consist of a semirigid tube with a short collapsible segment (the internal and external nasal valve). The portion of the internal nasal valve at the head of the inferior turbinate can be considered the upstream segment, whereas that portion posterior to the head of the inferior turbinate and the septal body is the downstream segment (Fig. 36.5). In other words, the semirigid tube conducts pressure changes to the collapsible segment, which is influenced by several factors including the conducted pressure, the extramural pressure, Bernoulli forces, and the elasticity of the collapsible cartilaginous segment. In the nose, negative inspiratory pressure is transmitted from the nasopharynx to the internal nasal valve area, which then narrows. The degree of narrowing depends on three variables:

In the normal nose, the nose does not collapse during quiet breathing because the tensile strength of the cartilage (upper lateral cartilage, lower lateral cartilage, and septal cartilage) support of the nose offsets the closing forces of the transmural pressure and the Bernoulli effect. The resistance to airflow is dependent on the skeletal (cartilage and bone) and mucocutaneous nasal structures that are anterior (upstream) and posterior (downstream) to the head of the inferior turbinate. At maximal inspiratory flow rates, a greater inspiratory effort (increased negative pressure) fails to increase airflow because the external nasal valve (ala) is collapsed (Fig. 36.6). The external nasal valve does not remain collapsed as the process is reversed during expiration.

The external nasal valve (ala) is really the airway opening supported by the paired lower lateral (great alar or alar) cartilages. The critical sites for collapse are either at the external nasal valve (lower lateral cartilage) or at the internal nasal valve (nasal valve area composed of the upper lateral cartilage, nasal septum, including the premaxillary wing region, floor of the nose, piriform aperture, and the head of the inferior turbinate). Some observers believe that the septal turbinate (septal “swell” body) is part of the nasal valve area and I tend to agree, but these findings tend to support the notion that total understanding the valve area and its function is still far from fully understood (Haight and Cole 1983; Huizing and de Groot 2003; Miman et al. 2006; Wexler and Davidson 2004). Nonetheless, it is necessary to have some practical understanding of the nasal valve area and its critical sites in order to perform surgery without disturbing nasal breathing function.

These critical sites are seen in Fig. 36.7. A clinical un-instrumented view of many of the structures of the internal and external nasal valve can be seen in Fig. 36.8. The alar muscles are also involved in valvular function and aid in preventing collapse of the valve at high inspiratory flow rates. Rigidity (scar) or flaccidity (over-resection) of cartilage structure including both the upper and the lower lateral cartilages and soft tissues would affect valvular function and breathing. Even minor changes in the diameter of the airway can significantly increase nasal airway resistance in concert with Poiseuille’s laws where the airflow is proportional to the pressure changes times the radius to the fourth power divided by the length. In other words, small changes in the radius to the fourth power are extremely significant.

Using acoustic rhinometry and active anterior rhinomanometry, Zambetti and associates (Zambetti et al. 2001) proved and supported the long-held clinical observation that small deformities in the anterior portion of the nose (upstream) like a scar in the valve angle can more profoundly and adversely effect nasal breathing than larger deformities in the interior of the nose (downstream) when they said, “Modest nasal cross-sectional area reductions posterior to the nasal valve do not cause substantial variations in nasal resistance…” (Zambetti et al. 2001).

The nasal valve area must function in concert with the structures upstream and downstream to provide nasal pulmonary respiratory balance over the wide range of physiologic demands. Since the head of the inferior turbinate is part of the internal nasal valve, it is affected by the vascular changes of the capacitance vessels in the stroma, which is termed the nasal cycle (Arbour and Kern 1975; Hasegawa and Kern 1977; Kern 1981). Actually the nasal cycle is a normal physiologic phenomenon that includes the alternating congestion and decongestion of the turbinates with changes in uninasal resistance while the total nasal resistance remains relatively constant (Fig. 36.9).

It is critical that nasal surgeons particularly rhinoplasty surgeons understand the pathophysiology of internal and external nasal valve since any disturbance in any portion of the critical sites in the nasal valve area (external valve and/or internal valve) can produce disturbed nasal breathing during exercise and/or at rest resulting in a very unhappy patient. The abnormalities responsible for nasal airway dysfunction include:

After blunt trauma (Barrs and Kern 1980), the second most likely cause of nasal valve abnormalities (with breathing problems) is nasal surgery (Barelli et al. 1987; Beekhuis 1976; Helal et al. 2010; Huizing and de Groot 2003; Nunez-Fernandez D 2999; Parkes and Kanodia 1981; Sheen 1983). Narrowing of the internal nasal valve angle by a medially displaced upper lateral cartilage after “hump” removal and infracture, additionally over-resection of the “hump” leaving an incomplete infracture, results in the “open roof” deformity (Barelli et al. 1987; Hinderer 1971; Javanbakht et al. 2012) and early collapse during inspiration in addition to posttraumatic neurogenic pain syndromes. Uncorrected septal pathology or over-resection of septal cartilage resulting in a “flaccid” septum with “flutter” is another cause of a collapsed internal nasal valve. Over-resection of the lower lateral cartilages may also result in “flaccid” collapse during inspiration. This “flaccid” collapse is also seen with loss of muscular action (as in facial paralysis) or with the atrophy of aging secondary to decreased tensile strength of the cartilages and soft tissues producing a “droopy tip” (Aksoy et al. 2010).

When rhinoplasty is considered, I take a considerable amount of time to develop a personal relationship (rapport) with the patient while obtaining a general medical history, supplemented with a rhinologic questionnaire (Kern 1972) which succinctly covers the essentials including a history of smoking and alcohol use, attention to allergic conditions (including seasonal and perennial allergic rhinitis, allergies to medications, soaps, surgical solutions, latex, tape), bleeding tendencies, use of steroids (topical and/or systemic), diabetes, hypertension, current and recent medications (including aspirin, aspirin-like drugs – nonsteroidal anti-inflammatory drugs), peripheral vascular disease, and previous operations of any kind.

In addition to physical nasal examination (looking for a Cottle sign Heinberg and Kern 1973) also use the endoscope (0 ° 4 mm) for an intranasal examination before and after topical decongestion to study the mucosa and the interior of the nose back to the nasopharynx. I usually obtain the following tests and consultations (when medically indicated):

I always ask for the patient’s parent(s) or significant other to be present before surgery, and I always welcome questions from the patient and family before ending the interview. The preoperative discussion is critical to establishing the necessary rapport with the patient and the family to better manage complications should they occur postoperatively. Succinctly, for cosmetic rhinoplasty, I ALWAYS discuss the following in detail: