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My study materials use the word vesselcompression chamber of aorta to emphasize aorta's elastic property.
The arch of the aorta only coils, not its straight part. I think the reason why the arch coils is the elasticity of aorta (artery) is high. If the elasticity is too low, then the aorta is more stiff. This means that heart has to work harder so higher systolic pressure and lower diastolic pressure.
Why does the arch of the aorta coils?
The main question can be answered in a very dumb way: because the lower part of the body also needs blood… and this configuration is the surest way of doing that because of reasons given below (among many others, I am sure).
If you want an anatomical reason, well the most pertinent one would be that embryologically, the heart and vascular system are derived from a single straight tube, that then begins contracting and folding over itself to form the heart chambers, the aorta, and the pulmonary trunk.
If you want a physiological explanation, the aorta curves slowly because it is a point of the circulatory system where pressure is high. Apart from the fact that sharp kinks would cause a massive and useless loss of kinetic energy on blood flow from shear stress over the aortic walls (and therefore more heart workload), the induced shear stress would also damage the aortic walls much more quickly than in the actual configuration.
The third reason is just theory on my part, but it seems the vascular system is designed by priorities: you could imagine a system with two aortas. One for the upper body going up, and a second going down. However, such a configuration makes it mechanically impossible to balance perfusion to the organs, and especially ensure brain perfusion. For example, how would the body compensate if the upper aorta got clogged while the other stayed wide open? The single aorta configuration allows the heart to adapt to such mechanical perturbation scenarii using, for example, left ventricular hypertrophy.
However to add to some elements of your question:
- the reason of the aortic coiling has certainly very little to do with elasticity and the vessel compression chamber principle.
- Higher elasticity means the aorta is less stiff, not more.
- When the aorta gets stiff (elasticity decreases) as it is often the case with age and calcification of the aortic walls, it is correct that the heart will need to work more, that systolic pressure will get higher, and diastolic pressure lower. This gives the classical clinical symptom of "cannonball" or "gunshot" pulse
The aorta is the largest artery in the body, initially being an inch wide in diameter. It receives the cardiac output from the left ventricle and supplies the body with oxygenated blood via the systemic circulation.
The aorta can be divided into four sections: the ascending aorta, the aortic arch, the thoracic (descending) aorta and the abdominal aorta. It terminates at the level of L4 by bifurcating into the left and right common iliac arteries. The aorta classified as a large elastic artery, and more information on its internal structure can be found here.
In this article we will look at the anatomy of the aorta – its anatomical course, branches and clinical correlations.
Fig 1 – Overview of the anatomical course of the aorta. By Edoarado [CC BY-SA 3.0], via Wikimedia Commons
Vascular Aneurysms and Dissections
M.K. Halushka , M.E. Lindsay , in Pathobiology of Human Disease , 2014
Aortic aneurysms (AAs) and dissections are rare but important causes of cardiovascular morbidity and mortality. Aneurysms can result from genetic predisposition in a Mendelian pattern in the young and old, as well as classical cardiovascular risk factors in older individuals. Despite elastic fiber fragmentation and pools of mucoid material being present in histopathologic specimens, in experimental murine models the causative mechanism for aneurysm progression appears to be altered transforming growth factor beta (TGF-β) activity driving functional deficiencies, rather than a primary structural derangement. Altered TGF-β activity has now been documented in human syndromic aneurysmal disease and in human nonsyndromic aneurysm. This article will describe the diseases and histopathologies of AA. It will also describe the mechanistic alterations in the TGF-β pathway as a result of genetic mutations and how these perturbations inform our understanding of AA development and progression.
I, just, come out of Emergency Room
with : Chest X report .
The report show Mild – aortic uncoiling.
Thanks for explanation on it.
I also learned that a chest x-ray showed that I have Uncoiling and tortuosity of the thoracic aorta. My doctor did not inform me of the condition, but when he retired my new doctor placed into the medical file that I had Atherosclerosis of Aorta. When I questioned her, she said the X-ray done in 2014 showed the Uncoiling and Tortuosity of the Thoracic. Please explain the difference between the two diagnoses.
I am going through the exact same thing right now. Went for chest xrays to determine or rule out pneumonia. Report says that I have “uncoiling of the aorta” indicative of hypertension.
I looked up hypertension. From what I’m reading, it doesn’t fit. I don’t have high blood pressure at all, and in fact, I have low blood pressure.
I was diagnosed last year with Bracacardia and I know I have a back flow issue and soem other minor things that may one day become major. But what is this uncoiling thing supposed to mean without high blood pressure! It’s quite confusing. Of course, I’ll be sending the report to my cardiologist for answers.
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Loeys BL, Schwarze U, Holm T, Callewaert BL, Thomas GH, Pannu H, De Backer JF, Oswald GL, Symoens S, Manouvrier S, Roberts AE, Faravelli F, Greco MA, Pyeritz RE, Milewicz DM, Coucke PJ, Cameron DE, Braverman AC, Byers PH, De Paepe AM, Dietz HC.
Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE, Eagle KA, Hermann LK, Isselbacher EM, Kazerooni EA, Kouchoukos NT, Lytle BW, Milewicz DM, Reich DL, Sen S, Shinn JA, Svensson LG, Williams DM.
Milewicz DM, Regalado ES, Guo DC.
Michelena HI, Khanna AD, Mahoney D, Margaryan E, Topilsky Y, Suri RM, Eidem B, Edwards WD, Sundt TM, Enriquez-Sarano M.
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Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, Picard MH, Roman MJ, Seward J, Shanewise JS, Solomon SD, Spencer KT, Sutton MS, Stewart WJ
Campens L, Demulier L, De Groote K, Vandekerckhove K, De Wolf D, Roman MJ, Devereux RB, De Paepe A, De Backer J.
D’Andrea A, Cocchia R, Riegler L, Scarafile R, Salerno G, Gravino R, Vriz O, Citro R, Limongelli G, Di Salvo G, Cuomo S, Caso P, Russo MG, Calabrò R, Bossone E.
Pelliccia A, Di Paolo FM, De Blasiis E, Quattrini FM, Pisicchio C, Guerra E, Culasso F, Maron BJ.
Pelliccia A, Di Paolo FM, Quattrini FM.
Reed CM, Richey PA, Pulliam DA, Somes GW, Alpert BS.
Hatzaras I, Tranquilli M, Coady M, Barrett PM, Bible J, Elefteriades JA.
Harris KM, Tung M, Haas TS, Maron BJ.
Parish LM, Gorman JH, Kahn S, Plappert T, St John-Sutton MG, Bavaria JE, Gorman RC.
Pape LA, Tsai TT, Isselbacher EM, Oh JK, O’Gara PT, Evangelista A, Fattori R, Meinhardt G, Trimarchi S, Bossone E, Suzuki T, Cooper JV, Froehlich JB, Nienaber CA, Eagle KA
Engelfriet PM, Boersma E, Tijssen JG, Bouma BJ, Mulder BJ.
Mimoun L, Detaint D, Hamroun D, Arnoult F, Delorme G, Gautier M, Milleron O, Meuleman C, Raoux F, Boileau C, Vahanian A, Jondeau G.
Kari FA, Fazel SS, Mitchell RS, Fischbein MP, Miller DC.
Maron BJ, Ackerman MJ, Nishimura RA, Pyeritz RE, Towbin JA, Udelson JE.
Kinoshita N, Mimura J, Obayashi C, Katsukawa F, Onishi S, Yamazaki H.
Bonow RO, Nishimura RA, Thompson PD, Udelson JEon behalf of the American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology, Council on Cardiovascular Disease in the Young, Council on Cardiovascular and Stroke Nursing, Council on Functional Genomics and Translational Biology, and the American College of Cardiology
Levine BD, Baggish AL, Kovacs RJ, Link MS, Maron MS, Mitchell JHon behalf of the American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology, Council on Cardiovascular Disease in the Young, Council on Cardiovascular and Stroke Nursing, Council on Functional Genomics and Translational Biology, and the American College of Cardiology
Aortic aneurysms are classified by their location on the aorta. [ citation needed ]
- An aortic root aneurysm, or aneurysm of the sinus of Valsalva. are found within the chest these are further classified as ascending, aortic arch, or descending aneurysms. , "AAA" or "Triple A", the most common form of aortic aneurysm, involve that segment of the aorta within the abdominal cavity. Thoracoabdominal aortic aneurysms involve both the thoracic and abdominal aorta.
- Thoracoabdominal aortic aneurysms comprise some or all of the aorta in both the chest and abdomen, and have components of both thoracic and abdominal aortic aneurysms.
Most intact aortic aneurysms do not produce symptoms. As they enlarge, symptoms such as abdominal pain and back pain may develop. Compression of nerve roots may cause leg pain or numbness. Untreated, aneurysms tend to become progressively larger, although the rate of enlargement is unpredictable for any individual. Rarely, clotted blood which lines most aortic aneurysms can break off and result in an embolus. [ citation needed ]
Aneurysms can be found on physical examination. Medical imaging is necessary to confirm the diagnosis and to determine the anatomic extent of the aneurysm. In patients presenting with aneurysm of the arch of the aorta, a common sign is a hoarse voice from stretching of the left recurrent laryngeal nerve, a branch of the vagus nerve that winds around the aortic arch to supply the muscles of the larynx. [ citation needed ]
Abdominal aortic aneurysm Edit
Abdominal aortic aneurysms (AAAs) are more common than their thoracic counterpart. One reason for this is that elastin, the principal load-bearing protein present in the wall of the aorta, is reduced in the abdominal aorta as compared to the thoracic aorta. Another is that the abdominal aorta does not possess vasa vasorum, the nutrient-supplying blood vessels within the wall of the aorta. Most AAA are true aneurysms that involve all three layers (tunica intima, tunica media and tunica adventitia). The prevalence of AAAs increases with age, with an average age of 65–70 at the time of diagnosis. AAAs have been attributed to atherosclerosis, though other factors are involved in their formation.
The risk of rupture of an AAA is related to its diameter once the aneurysm reaches about 5 cm, the yearly risk of rupture may exceed the risks of surgical repair for an average-risk patient. Rupture risk is also related to shape so-called "fusiform" (long) aneurysms are considered less rupture prone than "saccular" (shorter, bulbous) aneurysms, the latter having more wall tension in a particular location in the aneurysm wall. [ citation needed ]
Before rupture, an AAA may present as a large, pulsatile mass above the umbilicus. A bruit may be heard from the turbulent flow in the aneurysm. Unfortunately, however, rupture may be the first hint of AAA. Once an aneurysm has ruptured, it presents with classic symptoms of abdominal pain which is severe, constant, and radiating to the back. [ citation needed ]
The diagnosis of an abdominal aortic aneurysm can be confirmed at the bedside by the use of ultrasound. Rupture may be indicated by the presence of free fluid in the abdomen. A contrast-enhanced abdominal CT scan is the best test to diagnose an AAA and guide treatment options. [ citation needed ]
Only 10–25% of patients survive rupture due to large pre- and post-operative mortality. Annual mortality from ruptured aneurysms in the United States is about 15,000. Most are due to abdominal aneurysms, with thoracic and thoracoabdominal aneurysms making up 1% to 4% of the total. [ citation needed ]
Aortic rupture Edit
An aortic aneurysm can rupture from wall weakness. Aortic rupture is a surgical emergency, and has a high mortality even with prompt treatment. Weekend admission for ruptured aortic aneurysm is associated with an increased mortality compared with admission on a weekday, and this is likely due to several factors including a delay in prompt surgical intervention. 
Chronic Obstructive sleep apnoea syndrome
An aortic aneurysm can occur as a result of trauma, infection, or, most commonly, from an intrinsic abnormality in the elastin and collagen components of the aortic wall. While definite genetic abnormalities were identified in true genetic syndromes (Marfan, Elher-Danlos and others) associated with aortic aneurysms, both thoracic and abdominal aortic aneurysms demonstrate a strong genetic component in their aetiology. 
The risk of aneurysm enlargement may be diminished with attention to the patient's blood pressure, smoking and cholesterol levels. There have been proposals to introduce ultrasound scans as a screening tool for those most at risk: men over the age of 65.   The tetracycline antibiotic doxycycline is currently being investigated for use as a potential drug in the prevention of aortic aneurysm due to its metalloproteinase inhibitor and collagen stabilizing properties. [ citation needed ]
Anacetrapib is a cholesteryl ester transfer protein inhibitor that raises high-density lipoprotein (HDL) cholesterol and reduces low-density lipoprotein (LDL) cholesterol. Anacetrapib reduces progression of atherosclerosis, mainly by reducing non-HDL-cholesterol, improves lesion stability and adds to the beneficial effects of atorvastatin  Elevating the amount of HDL cholesterol in the abdominal area of the aortic artery in mice both reduced the size of aneurysms that had already grown and prevented abdominal aortic aneurysms from forming at all. In short, raising HDL cholesterol is beneficial because it induces programmed cell death. The walls of a failing aorta are replaced and strengthened. New lesions should not form at all when using this drug. 
Screening for an aortic aneurysm so that it may be detected and treated prior to rupture is the best way to reduce the overall mortality of the disease. The most cost-efficient screening test is an abdominal aortic ultrasound study. Noting the results of several large, population-based screening trials, the US Centers for Medicare and Medicaid Services (CMS) now provides payment for one ultrasound study in male or female smokers aged 65 years or older ("SAAAVE Act"). [ citation needed ]
Surgery (open or endovascular) is the definitive treatment of an aortic aneurysm. Medical therapy is typically reserved for smaller aneurysms or for elderly, frail patients where the risks of surgical repair exceed the risks of non-operative therapy (observation alone).
Medical therapy Edit
Medical therapy of aortic aneurysms involves strict blood pressure control. This does not treat the aortic aneurysm per se, but control of hypertension within tight blood pressure parameters may decrease the rate of expansion of the aneurysm.
The medical management of patients with aortic aneurysms, reserved for smaller aneurysms or frail patients, involves cessation of smoking, blood pressure control, use of statins and occasionally beta blockers. Ultrasound studies are obtained on a regular basis (i.e. every six or 12 months) to follow the size of the aneurysm.
Despite optimal medical therapy, patients with large aneurysms are likely to have continued aneurysm growth and risk of aneurysm rupture without surgical repair. 
Decisions about repairing an aortic aneurysm are based on the balance between the risk of aneurysm rupture without treatment versus the risks of the treatment itself. For example, a small aneurysm in an elderly patient with severe cardiovascular disease would not be repaired. The chance of the small aneurysm rupturing is overshadowed by the risk of cardiac complications from the procedure to repair the aneurysm.
The risk of the repair procedure is two-fold. First, there is consideration of the risk of problems occurring during and immediately after the procedure itself ("peri-procedural" complications). Second, the effectiveness of the procedure must be taken into account, namely whether the procedure effectively protects the patient from aneurysm rupture over the long-term, and whether the procedure is durable so that secondary procedures, with their attendant risks, are not necessary over the life of the patient. A less invasive procedure (such as endovascular aneurysm repair) may be associated with fewer short-term risks to the patient (fewer peri-procedural complications) but secondary procedures may be necessary over long-term follow-up.
The determination of surgical intervention is determined on a per-case basis. The diameter of the aneurysm, its rate of growth, the presence or absence of Marfan syndrome, Ehlers–Danlos syndromes or similar connective tissue disorders, and other co-morbidities are all important factors in the overall treatment.
A large, rapidly expanding, or symptomatic aneurysm should be repaired, as it has a greater chance of rupture. Slowly expanding aortic aneurysms may be followed by routine diagnostic testing (i.e.: CT scan or ultrasound imaging).
For abdominal aneurysms, the current treatment guidelines for abdominal aortic aneurysms suggest elective surgical repair when the diameter of the aneurysm is greater than 5 cm (2 in). However, recent data on patients aged 60–76 suggest medical management for abdominal aneurysms with a diameter of less than 5.5 cm (2 in). 
Open surgery Edit
Open surgery starts with exposure of the dilated portion of the aorta via an incision in the abdomen or abdomen and chest, followed by insertion of a synthetic (Dacron or Gore-Tex) graft (tube) to replace the diseased aorta. The graft is sewn in by hand to the non-diseased portions of the aorta, and the aneurysmal sac is closed around the graft.
The aorta and its branching arteries are cross-clamped during open surgery. This can lead to inadequate blood supply to the spinal cord, resulting in paraplegia. A 2004 systematic review and meta analysis found that cerebrospinal fluid drainage (CFSD), when performed in experienced centers, reduces the risk of ischemic spinal cord injury by increasing the perfusion pressure to the spinal cord.  A 2012 Cochrane systematic review noted that further research regarding the effectiveness of CFSD for preventing a spinal cord injury is required. 
Endovascular treatment of aortic aneurysms is a minimally invasive alternative to open surgery repair. It involves placement of an endo-vascular stent through small incisions at the top of each leg into the aorta.
As compared to open surgery, EVAR has a lower risk of death in the short term and a shorter hospital stay but may not always be an option.    There does not appear to be a difference in longer term outcomes between the two.  After EVAR, repeat procedures are more likely to be needed. 
Aortic aneurysms resulted in about 152,000 deaths in 2013 up from 100,000 in 1990. 
In vertebrates, the pharyngeal arches are derived from all three germ layers (the primary layers of cells that form during embryogenesis).  Neural crest cells enter these arches where they contribute to features of the skull and facial skeleton such as bone and cartilage.  However, the existence of pharyngeal structures before neural crest cells evolved is indicated by the existence of neural crest-independent mechanisms of pharyngeal arch development.  The first, most anterior pharyngeal arch gives rise to the oral jaw. The second arch becomes the hyoid and jaw support.  In fish, the other posterior arches contribute to the branchial skeleton, which support the gills in tetrapods the anterior arches develop into components of the ear, tonsils, and thymus.  The genetic and developmental basis of pharyngeal arch development is well characterized. It has been shown that Hox genes and other developmental genes such as DLX are important for patterning the anterior/posterior and dorsal/ventral axes of the branchial arches.  Some fish species have a second set of jaws in their throat, known as pharyngeal jaws, which develop using the same genetic pathways involved in oral jaw formation. 
During human and all vertebrate development, a series of pharyngeal arch pairs form in the developing embryo. These project forward from the back of the embryo toward the front of the face and neck. Each arch develops its own artery, nerve that controls a distinct muscle group, and skeletal tissue. The arches are numbered from 1 to 6, with 1 being the arch closest to the head of the embryo, and arch 5 existing only transiently. 
These grow and join in the ventral midline. The first arch, as the first to form, separates the mouth pit or stomodeum from the pericardium. By differential growth the neck elongates and new arches form, so the pharynx has six arches ultimately.
Each pharyngeal arch has a cartilaginous stick, a muscle component that differentiates from the cartilaginous tissue, an artery, and a cranial nerve. Each of these is surrounded by mesenchyme. Arches do not develop simultaneously but instead possess a "staggered" development.
Pharyngeal pouches form on the endodermal side between the arches, and pharyngeal grooves (or clefts) form from the lateral ectodermal surface of the neck region to separate the arches.  In fish the pouches line up with the clefts, and these thin segments become gills. In mammals the endoderm and ectoderm not only remain intact but also continue to be separated by a mesoderm layer.
The development of the pharyngeal arches provides a useful landmark with which to establish the precise stage of embryonic development. Their formation and development corresponds to Carnegie stages 10 to 16 in mammals, and Hamburger–Hamilton stages 14 to 28 in the chicken. Although there are six pharyngeal arches, in humans the fifth arch exists only transiently during embryogenesis. 
The first pharyngeal arch also mandibular arch (corresponding to the first branchial arch or gill arch of fish), is the first of six pharyngeal arches that develops during the fourth week of development.  It is located between the stomodeum and the first pharyngeal groove.
This arch divides into a maxillary process and a mandibular process, giving rise to structures including the bones of the lower two-thirds of the face and the jaw. The maxillary process becomes the maxilla (or upper jaw), and palate while the mandibular process becomes the mandible or lower jaw. This arch also gives rise to the muscles of mastication.
Meckel's cartilage Edit
Meckel's cartilage forms in the mesoderm of the mandibular process and eventually regresses to form the incus and malleus of the middle ear, the anterior ligament of the malleus and the sphenomandibular ligament. The mandible or lower jaw forms by perichondral ossification using Meckel's cartilage as a 'template', but the maxillary does not arise from direct ossification of Meckel's cartilage.
The skeletal elements and muscles are derived from mesoderm of the pharyngeal arches.
Mucous membrane and glands of the anterior two thirds of the tongue are derived from ectoderm and endoderm of the arch.
Nerve supply Edit
The mandibular and maxillary branches of the trigeminal nerve (CN V) innervate the structures derived from the corresponding processes of the first arch. In some lower animals, each arch is supplied by two cranial nerves. The nerve of the arch itself runs along the cranial side of the arch and is called post-trematic nerve of the arch. Each arch also receives a branch from the nerve of the succeeding arch called the pre-trematic nerve which runs along the caudal border of the arch. In human embryo, a double innervation is seen only in the first pharyngeal arch. The mandibular nerve is the post-trematic nerve of the first arch and chorda tympani (branch of facial nerve) is the pre-trematic nerve. This double innervation is reflected in the nerve supply of anterior two-thirds of tongue which is derived from the first arch. 
Blood supply Edit
The artery of the first arch is the first aortic arch,  which partially persists as the maxillary artery.
The second pharyngeal arch or hyoid arch, is the second of fifth pharyngeal arches that develops in fetal life during the fourth week of development  and assists in forming the side and front of the neck.
Reichert's cartilage Edit
Cartilage in the second pharyngeal arch is referred to as Reichert's cartilage and contributes to many structures in the fully developed adult.  In contrast to the Meckel's cartilage of the first pharyngeal arch it does not constitute a continuous element, and instead is composed of two distinct cartilaginous segments joined by a faint layer of mesenchyme.  Dorsal ends of Reichert's cartilage ossify during development to form the stapes of the middle ear before being incorporated into the middle ear cavity, while the ventral portion ossifies to form the lesser cornu and upper part of the body of the hyoid bone. Caudal to what will eventually become the stapes, Reichert's cartilage also forms the styloid process of the temporal bone. The cartilage between the hyoid bone and styloid process will not remain as development continues, but its perichondrium will eventually form the stylohyoid ligament.
From the cartilage of the second arch arises
Nerve supply Edit
Blood supply Edit
The artery of the second arch is the second aortic arch,  which gives origin to the stapedial artery in some mammals but atrophies in humans.
Pharyngeal muscles or Brancial muscles are striated muscles of the head and neck. Unlike skeletal muscles that developmentally come from somites, pharyngeal muscles are developmentally formed from the pharyngeal arches.
Most of the skeletal musculature supplied by the cranial nerves (special visceral efferent) is pharyngeal. Exceptions include, but are not limited to, the extraocular muscles and some of the muscles of the tongue. These exceptions receive general somatic efferent innervation.
First arch Edit
All of the pharyngeal muscles that come from the first pharyngeal arch are innervated by the mandibular divisions of the trigeminal nerve.  These muscles include all the muscles of mastication, the anterior belly of the digastric, the mylohyoid, tensor tympani, and tensor veli palatini.
Second arch Edit
All of the pharyngeal muscles of the second pharyngeal arch are innervated by the facial nerve. These muscles include the muscles of facial expression, the posterior belly of the digastric, the stylohyoid muscle, the auricular muscle  and the stapedius muscle of the middle ear.
Third arch Edit
There is only one muscle of third pharyngeal arch, the stylopharyngeus. The stylopharyngeus and other structures from the third pharyngeal arch are all innervated by the glossopharyngeal nerve.
Fourth and sixth arches Edit
All the pharyngeal muscles of the fourth and sixth arches are innervated by the superior laryngeal and the recurrent laryngeal branches of the vagus nerve.  These muscles include all the muscles of the palate (exception of the tensor veli palatini which is innervated by the trigeminal nerve), all the muscles of the pharynx (except stylopharyngeus which is innervated by the glossopharyngeal nerve), and all the muscles of the larynx.
Since no human structures result from the fifth arch, the arches in humans are I, II, III, IV, and VI.  More is known about the fate of the first arch than the remaining four. The first three contribute to structures above the larynx, whereas the last two contribute to the larynx and trachea.
The recurrent laryngeal nerves are produced from the nerve of arch 6, and the laryngeal cartilages from arches 4 and 6. The superior laryngeal branch of the vagus nerve arises from arch 4. Its arteries, which project between the nerves of the fourth and sixth arches, become the left-side arch of the aorta and the right subclavian artery. On the right side, the artery of Arch 6 is obliterated while, on the left side, the artery persists as the ductus arteriosus circulatory changes immediately following birth cause the vessel to close down, leaving a remnant, the ligamentum arteriosum. During growth, these arteries descend into their ultimate positions in the chest, creating the elongated recurrent paths. 
Rat - Circulatory System
The general structure of the circulatory system of the rat is almost identical to that of humans. Pulmonary circulation carries blood through the lungs for oxygenation and then back to the heart. Systemic circulation moves blood through the body after it has left the heart. You will begin your dissection at the heart. It is important that you do not cut the vessels as you carefully remove any muscles and surrounding tissue to expose them. Your rat should be double injected so that arteries and veins are visible as blue and pink.
Trace the Flow of Blood Inside the Heart
The heart of the rat is too small to view many of the structures listed below. Use models of human hearts or images in the dissection guides to identify the structures and label them on the diagram.
1. Blood from the posterior portion of the body enters the right atrium of the heart through the inferior vena cava and the superior vena cava.
2. Blood flows from the right atrium to the right ventricle via the tricuspid valve.
3. Blood is then pumped through the pulmonary semilunar valve and into the pulmonary trunk where blood travels to the lungs.
4. Blood then flows through the pulmonary arteries to the lungs where it is oxygenated and then returns from the lungs to enter the left atrium via four pulmonary veins. Only one of these is visible on the diagram, a tiny vessel on the right side.
5. Blood goes from the left atrium to the left ventricle via the bicuspid (or mitral) valve.
6. Blood leaves the left ventricle of the heart through the aortic semilunar valve and enters the aorta. The aorta has a visible arch with vessels that lead to the head before the artery descends into the rat's thoracic cavity.
Label the diagram using the descriptions and bold words. Trace the flow of blood using arrows.
Branches of the Aorta
The aorta has four general areas. Locate each of these on your rat.
ascending aorta - the upper part of the vessel that starts at the atrium
aortic arch - the place where the aorta bends to the left.
descending aorta - after the bend, the aorta can be traced toward the diaphragm
abdominal aorta - the aorta passes through the diaphragm and supplies blood to the lower extremities
1. Coronary arteries are located on top of the heart and supply the heart itself with blood.
2. The first visible branch from the aorta is the brachiocephalic artery, it divides into the right common carotid artery, which supplies the right side of the neck, and the right subclavian artery, which supplies the right shoulder and arms. Locate the carotid arteries on your rat, they will be obvious arteries that travel up the side of the next.
3. At the most anterior part of the bend in the aortic arch is the left common carotid artery, which supplies blood up the left side of the neck. If you are careful you can follow the common carotid to where it branches into the internal and external carotid.
4. Immediately to the left of the left common carotid artery is the left subclavian artery, which supplies blood to the left shoulder and arm. The sublclavian artery becomes the axillary artery as it enters the forearm.
Procedure: Carefully tease away the muscles and tissue so that the subclavian, the axillary and the right common carotid can be seen.
Trace The Branches of the Abdominal Aorta
Many of the arteries that branch from the aorta in this part of the rat are small and fragile. You may not be able to find all of them, but with careful dissection a few can be exposed. They are often named for the organ or structure the vessel supplies blood to. Find at least three of the vessels listed for your checkpoint. If you cannot find the vessel, do not check the box.
1. The first arterial branch from the abdominal aorta (below the diaphragm) is the celiac artery which branches to arteries that supply the stomach (gastric artery), liver (hepatic artery), spleen and pancreas (splenic artery) .
2. The second artery arising from the abdominal artery is the superior mesenteric artery, which is larger than the celiac, and delivers blood directly to the small intestine.
3. The renal arteries are short and lead directly to the kidneys. These are probably the easiest to locate.
4. Just posterior to the renal arteries are the genital arteries, which lead to the testes or the ovaries.
5. Farther along the abdominal aorta, you can find the iliolumbar arteries which lead to the dorsal muscles of the back.
6. Next, the inferior mesenteric artery leads to the intestinal mesenteries.
7. The abdominal aorta gives rise to the caudal artery, which goes on into the tail.
8. The abdominal aorta finally divides to form the iliac arteries, which deliver blood to the pelvis and hind legs.
9. The iliac arteries lead to the femoral artery in the leg.
Procedure:Attempt to locate the vessels above, find at least three of them.
Trace the Systemic Veins
1. The left and right superior vena cava conduct blood from the upper part of the body into the right atrium. Trace these veins from the atrium until you find the small internal jugular vein and continues as the subclavian vein.
2. The subclavian vein divides into the external jugular vein and the axillary vein.
3. The inferior vena cava carries blood from the lower part of the body to the right atrium. The hepatic vein drains the liver and enters the inferior vena cava near the diaphragm.
4. Renal veins drain the kidneys.
5. Genital veins lead from the gonads and enter the inferior vena cava.
6. The iliac and femoral veins drain the legs.
7. The caudal vein drains the tail.
Procedure: Expose the inferior vena cava and the area where it branches into the femoral and caudal veins.
Aneurysms are classified by type, morphology, or location.
True and false aneurysms Edit
A true aneurysm is one that involves all three layers of the wall of an artery (intima, media and adventitia). True aneurysms include atherosclerotic, syphilitic, and congenital aneurysms, as well as ventricular aneurysms that follow transmural myocardial infarctions (aneurysms that involve all layers of the attenuated wall of the heart are also considered true aneurysms). 
A false aneurysm, or pseudoaneurysm, is a collection of blood leaking completely out of an artery or vein, but confined next to the vessel by the surrounding tissue. This blood-filled cavity will eventually either thrombose (clot) enough to seal the leak, or rupture out of the surrounding tissue.  : 357
Pseudoaneurysms can be caused by trauma that punctures the artery, such as knife and bullet wounds,  as a result of percutaneous surgical procedures such as coronary angiography or arterial grafting,  or use of an artery for injection. 
Aneurysms can also be classified by their macroscopic shapes and sizes and are described as either saccular or fusiform. The shape of an aneurysm is not specific for a specific disease.  : 357 The size of the base or neck is useful in determining the chance of for example endovascular coiling. 
Saccular aneurysms, or "berry" aneurysms, are spherical in shape and involve only a portion of the vessel wall they usually range from 5 to 20 cm (2.0 to 7.9 in) in diameter, and are often filled, either partially or fully, by a thrombus.  : 357 Saccular aneurysms have a "neck” that connects the aneurysm to its main ("parent") artery, a larger, rounded area, called the dome.
Fusiform aneurysms ("spindle-shaped" aneurysms) are variable in both their diameter and length their diameters can extend up to 20 cm (7.9 in). They often involve large portions of the ascending and transverse aortic arch, the abdominal aorta, or, less frequently, the iliac arteries.  : 357
Aneurysms can also be classified by their location:
- and venous, with arterial being more common. 
- The heart, including coronary artery aneurysms, ventricular aneurysms, aneurysm of sinus of Valsalva, and aneurysms following cardiac surgery.
- The aorta, namely aortic aneurysms including thoracic aortic aneurysms and abdominal aortic aneurysms. 
- The brain, including cerebral aneurysms, berry aneurysms, and Charcot–Bouchard aneurysms.
- The legs, including the popliteal arteries. 
- The kidney, including renal artery aneurysm and intraparechymal aneurysms.  , specifically capillary aneurysms.
- The Large vessels such as external and internal jugular veins 
Cerebral aneurysms, also known as intracranial or brain aneurysms, occur most commonly in the anterior cerebral artery, which is part of the circle of Willis. This can cause severe strokes leading to death. The next most common sites of cerebral aneurysm occurrence are in the internal carotid artery. 
|Ectatic or |
|>2.0 cm and <3.0 cm |
|Moderate||3.0–5.0 cm |
|Large or severe||>5.0  or 5.5  cm|
Abdominal aortic aneurysms are commonly divided according to their size and symptomatology. An aneurysm is usually defined as an outer aortic diameter over 3 cm (normal diameter of the aorta is around 2 cm),  or more than 50% of normal diameter that of a healthy individual of the same sex and age.   If the outer diameter exceeds 5.5 cm, the aneurysm is considered to be large. 
|Normal||Diameter ≤12 mm|
|Ectatic||Diameter 12 to 18 mm|
|Aneurysm||Diameter ≥18 mm|
Aneurysm presentation may range from life-threatening complications of hypovolemic shock to being found incidentally on X-ray.  Symptoms will differ by the site of the aneurysm and can include:
Cerebral aneurysm Edit
Symptoms can occur when the aneurysm pushes on a structure in the brain. Symptoms will depend on whether an aneurysm has ruptured or not. There may be no symptoms present at all until the aneurysm ruptures.  For an aneurysm that has not ruptured the following symptoms can occur:
For a ruptured aneurysm, symptoms of a subarachnoid hemorrhage may present:
- Severe headaches
- Loss of vision
- Double vision
- Neck pain or stiffness
- Pain above or behind the eyes
Abdominal aneurysm Edit
Abdominal aortic aneurysm involves a regional dilation of the aorta and is diagnosed using ultrasonography, computed tomography, or magnetic resonance imaging. A segment of the aorta that is found to be greater than 50% larger than that of a healthy individual of the same sex and age is considered aneurysmal.  Abdominal aneurysms are usually asymptomatic but in rare cases can cause lower back pain or lower limb ischemia.
Renal (kidney) aneurysm Edit
- Flank pain and tenderness
- Signs of hypovolemic shock
Risk factors for an aneurysm include diabetes, obesity, hypertension, tobacco use, alcoholism, high cholesterol, copper deficiency, increasing age, and tertiary syphilis infection.  : 602 Connective tissue disorders such as Loeys-Dietz syndrome, Marfan syndrome, and certain forms of Ehlers-Danlos syndrome are also associated with aneurysms. Aneurysms, dissections, and ruptures in individuals under 40 years of age are a major diagnostic criteria of the vascular form of Ehlers-Danlos syndrome (vEDS). 
Specific infective causes associated with aneurysm include:
A minority of aneurysms are associated with genetic factors. Examples include:
Aneurysms form for a variety of interacting reasons. Multiple factors, including factors affecting a blood vessel wall and the blood through the vessel, contribute.
The pressure of blood within the expanding aneurysm may also injure the blood vessels supplying the artery itself, further weakening the vessel wall. Without treatment, these aneurysms will ultimately progress and rupture. 
Infection. A mycotic aneurysm is an aneurysm that results from an infectious process that involves the arterial wall.  A person with a mycotic aneurysm has a bacterial infection in the wall of an artery, resulting in the formation of an aneurysm. The most common locations include arteries in the abdomen, thigh, neck, and arm. A mycotic aneurysm can result in sepsis, or life-threatening bleeding if the aneurysm ruptures. Less than 3% of abdominal aortic aneurysms are mycotic aneurysms. 
Syphilis. The third stage of syphilis also manifests as aneurysm of the aorta, which is due to loss of the vasa vasorum in the tunica adventitia. 
Copper deficiency. A minority of aneurysms are caused by copper deficiency, which results in a decreased activity of the lysyl oxidase enzyme, affecting elastin, a key component in vessel walls.    Copper deficiency results in vessel wall thinning,  and thus has been noted as a cause of death in copper-deficient humans,  chickens, and turkeys. 
Aneurysmal blood vessels are prone to rupture under normal blood pressure and flow due to their special mechanical properties that make them weaker. To better understand this phenomenon, we can first look at healthy arterial vessels which exhibit a J-shaped stress-strain curve with high strength and high toughness (for a biomaterial in vivo).  Unlike crystalline materials whose linear elastic region follows Hooke's Law under uniaxial loading, many biomaterials exhibit a J-shaped stress-strain curve which is non-linear and concave up.  The blood vessel can be under large strain, or the amount of stretch the blood vessel can undergo, for a range of low applied stress before fracture, as shown by the lower part of the curve. The area under the curve up to a given strain is much lower than that for the equivalent Hookean curve, which is correlated to toughness. Toughness is defined as the amount of energy per unit volume a material can absorb before rupturing. Because the amount of energy release is proportional to the amount of crack propagation, the blood vessel wall can withstand pressure and is “tough.” Thus, healthy blood vessels with the mechanical properties of the J-shaped stress-strain curve have greater stability against aneurysms than materials with linear elasticity.
Blood vessels with aneurysms, on the other hand, are under the influence of an S-shaped stress-strain curve. As a visual aid, aneurysms can be understood as a long, cylindrical balloon. Because it's a tight balloon under pressure, it can pop at any time a stress beyond a certain force threshold is applied. In the same vein, an unhealthy blood vessel has elastic instabilities that lead to rupture.  Initially, for a given radius and pressure, stiffness of the material increases linearly. At a certain point, the stiffness of the arterial wall starts to decrease with increasing load. At higher strain values, the area under the curve increases, thus increasing the impact on the material that would promote crack propagation. The differences in the mechanical properties of the aneurysmal blood vessels and the healthy blood vessels stem from the compositional differences of the vessels. Compared to normal aortas, aneurysmal aortas have a much higher volume fraction of collagen and ground substance (54.8% vs. 95.6%) and a much lower volume fraction of elastin (22.7% vs. 2.4%) and smooth muscles (22.6% vs. 2.2%), which contribute to higher initial stiffness.  It was also found that the ultimate tensile strength, or the strength to withstand rupture, of aneurysmal vessel wall is 50% lower than that of normal aortas.  The wall strength of ruptured aneurysmal aortic wall was also found to be 54.2 N/cm 2 , which is much lower than that of a repaired aorta wall, 82.3 N/cm 2 .  Due to the change in composition of the arterial wall, aneurysms overall have much lower strength to resist rupture. Predicting the risk of rupture is difficult due to the regional anisotropy the hardened blood vessels exhibit, meaning that the stress and strength values vary depending on the region and the direction of the vessel they are measured along. 
Diagnosis of a ruptured cerebral aneurysm is commonly made by finding signs of subarachnoid hemorrhage on a computed tomography (CT) scan. If the CT scan is negative but a ruptured aneurysm is still suspected based on clinical findings, a lumbar puncture can be performed to detect blood in the cerebrospinal fluid. Computed tomography angiography (CTA) is an alternative to traditional angiography and can be performed without the need for arterial catheterization. This test combines a regular CT scan with a contrast dye injected into a vein. Once the dye is injected into a vein, it travels to the cerebral arteries, and images are created using a CT scan. These images show exactly how blood flows into the brain arteries. [ citation needed ]
Historically, the treatment of arterial aneurysms has been limited to either surgical intervention, or watchful waiting in combination with control of blood pressure. At least, in case of abdominal aortic aneurysm (AAA) the decision does not come without a significant risk and cost, hence, there is a great interest in identifying more advanced decision making approaches that are not solely based on the AAA diameter, but involve other geometrical and mechanical nuances such as local thickness and wall stress.  In recent years, [ when? ] endovascular or minimally invasive techniques have been developed for many types of aneurysms. Aneurysm clips are used for surgical procedure i.e. clipping of aneurysms. 
There are currently two treatment options for brain aneurysms: surgical clipping or endovascular coiling. There is currently debate in the medical literature about which treatment is most appropriate given particular situations. 
Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937. It consists of a craniotomy to expose the aneurysm and closing the base or neck of the aneurysm with a clip. The surgical technique has been modified and improved over the years.
Endovascular coiling was introduced by Italian neurosurgeon Guido Guglielmi at UCLA in 1989. It consists of passing a catheter into the femoral artery in the groin, through the aorta, into the brain arteries, and finally into the aneurysm itself. Platinum coils initiate a clotting reaction within the aneurysm that, if successful, fills the aneurysm dome and prevents its rupture.  A flow diverter can be used, but risks complications. 
Aortic and peripheral Edit
For aneurysms in the aorta, arms, legs, or head, the weakened section of the vessel may be replaced by a bypass graft that is sutured at the vascular stumps. Instead of sewing, the graft tube ends, made rigid and expandable by nitinol wireframe, can be easily inserted in its reduced diameter into the vascular stumps and then expanded up to the most appropriate diameter and permanently fixed there by external ligature.   New devices were recently developed to substitute the external ligature by expandable ring allowing use in acute ascending aorta dissection, providing airtight (i.e. not dependent on the coagulation integrity), easy and quick anastomosis extended to the arch concavity    Less invasive endovascular techniques allow covered metallic stent grafts to be inserted through the arteries of the leg and deployed across the aneurysm.
Renal aneurysms are very rare consisting of only 0.1–0.09%  while rupture is even more rare.   Conservative treatment with control of concomitant hypertension being the primary option with aneurysms smaller than 3 cm. If symptoms occur, or enlargement of the aneurysm, then endovascular or open repair should be considered.  Pregnant women (due to high rupture risk of up to 80%) should be treated surgically. 
Incidence rates of cranial aneurysms are estimated at between 0.4% and 3.6%. Those without risk factors have expected prevalence of 2–3%.  : 181 In adults, females are more likely to have aneurysms. They are most prevalent in people ages 35 – 60, but can occur in children as well. Aneurysms are rare in children with a reported prevalence of .5% to 4.6%. The most common incidence are among 50-year-olds, and there are typically no warning signs. Most aneurysms develop after the age of 40. [ citation needed ]
Pediatric aneurysms Edit
Pediatric aneurysms have different incidences and features than adult aneurysms.  Intracranial aneurysms are rare in childhood, with over 95% of all aneurysms occurring in adults.  : 235
Risk factors Edit
Incidence rates are two to three times higher in males, while there are more large and giant aneurysms and fewer multiple aneurysms.  : 235 Intracranial hemorrhages are 1.6 times more likely to be due to aneurysms than cerebral arteriovenous malformations in whites, but four times less in certain Asian populations.  : 235
Most patients, particularly infants, present with subarachnoid hemorrhage and corresponding headaches or neurological deficits. The mortality rate for pediatric aneurysms is lower than in adults.  : 235
Modeling of aneurysms consists of creating a 3D model that mimics a particular aneurysm. Using patient data for the blood velocity, and blood pressure, along with the geometry of the aneurysm, researchers can apply computational fluid dynamics (CFD) to predict whether an aneurysm is benign or if it is at risk of complication. One risk is rupture. Analyzing the velocity and pressure profiles of the blood flow leads to obtaining the resulting wall shear stress on the vessel and aneurysm wall. The neck of the aneurysm is the most at risk due to the combination of a small wall thickness and high wall shear stress. When the wall shear stress reaches its limit, the aneurysm ruptures, leading to intracranial hemorrhage. Conversely, another risk of aneurysms is the creation of clots. Aneurysms create a pocket which diverts blood flow. This diverted blood flow creates a vortex inside of the aneurysm. This vortex can lead to areas inside of the aneurysm where the blood flow is stagnant, which promotes formations of clots. Blood clots can dislodge from the aneurysm, which can then lead to an embolism when the clot gets stuck and disrupts blood flow. Model analysis allows these risky aneurysms to be identified and treated.    
In the past, aneurysms were modeled as rigid spheres with linear inlets and outlets. As technology advances, the ability to detect and analyze aneurysms becomes easier. Researchers are able to CT scan a patient's body to create a 3D computer model that possesses the correct geometry. Aneurysms can now be modeled with their distinctive "balloon" shape. Nowadays researchers are optimizing the parameters required to accurately model a patient's aneurysm that will lead to a successful intervention. Current modeling is not able to take into account all variables though. For example, blood is considered to be a non-Newtonian fluid. Some researchers treat blood as a Newtonian fluid instead, as it sometimes has negligible effects to the analysis in large vessels. When analyzing small vessels though, such as those present in intracranial aneurysms. Similarly, sometimes it is difficult to model the varying wall thickness in small vessels, so researchers treat wall thickness as constant. Researchers make these assumptions to reduce computational time. Nonetheless, making erroneous assumptions could lead to a misdiagnosis that could put a patient's life at risk.    
Aortic Aneurysm Prognosis
Prognosis is usually good when an aortic aneurysm is treated before it ruptures.
Treatment and Recovery
Treatment for an aortic aneurysm depends on its size, location and your overall health. Once an aortic aneurysm has been diagnosed, our goal is to develop an individualized plan to treat it so it will not develop to a dangerous level and rupture. Depending on the size of the aortic aneurysm, treatment can include:
If the size of the aortic aneurysm is small, medication may be used to slow its growth rate. It is imperative that your blood pressure be monitored and blood pressure medication be taken as prescribed. A statin medication, which lowers cholesterol and can help keep your blood vessels healthy, may also be prescribed. Regular testing is an important way to keep a watchful eye on the aneurysm.
The most effective treatment for a larger, fast-growing or leaking aneurysm is surgery. You may be recommended for aortic aneurysm repair via traditional open surgery or a less invasive procedure called endovascular surgery. The type of procedure recommended for you depends upon the location and appearance of the aneurysm and your health.
During open surgery, the weakened section of the vessel will be removed and replaced with a graft. If the aneurysm is close to the aortic valve (the valve that regulates blood flow from the heart into the aorta), a valve replacement may also be recommended during the procedure.
During endovascular surgery, a stent graft is positioned inside the diseased section of the aorta. The stent acts as a liner to divert blood flow away from the aneurysm.
Recovery After Surgery
Depending upon how your body heals, you will be in the hospital for up to 10 days after open surgery and it may be three to six months before you feel able to fully resume your normal activities. After endovascular surgery, you will be in the hospital for a few days and it may be four to six weeks before you fully recover.
If an aortic aneurysm is not diagnosed and treated, the aneurysm could cause serious health problems. Those problems can include:
Rupture: Because the aorta is the main supplier of blood to the body, a rupture could cause life-threatening bleeding. This creates an emergency surgical situation.
Blood clots: Blood clots can weaken the heart and affect its ability to pump blood through the body. If a blood clot breaks loose, it could block a blood vessel anywhere in your body.