Pathophysiologyof the chronic venous insufficiency (CVI)

CVIis a condition that leads to feet and legs swelling, the pressurebuild up causes closure in the valves which in return causes theswelling of legs, varicose vein and skin discoloration. On the otherhand, DVT is a blood clot that develops in the vein deep in the bodythat blocks the blood flow in the vein.

Chronicvenous disease has become a very serious problem in the modern world.This disease is very crucial since it can resultin major morbidityand mortality. The most common way that leads to chronic venousinsufficiency is the development of venous hypertension which inmost cases is caused by obstruction of venous flow, dysfunctionof venous valves or failure of the venous pump. When such cases occur, flow is directed abnormally from the deep to the superficial system hence producing local tissue inflammationfibrosis and occasionally ulceration (Valji, &amp Valji, 2012).

The following are the major vascular pathways that are responsible for draining blood away from the superficial vessels of the skinand subcutaneous fat. Superficial veins-This are superficialveins that are deep to the muscular fascia and include the great and small saphenous veins. The second pathway is the deepveins which are located deep to the muscle fascia. These veins areeither within the muscle or between the muscles. The veins that arelocated within the muscles are regarded to be more important in thedevelopment of chronic venous insufficiency.

Pathophysiologyof Deep Vein Thrombosis (DVT)

Perforating veins are also vascular pathways and this veins communicate between the deep and superficial systems. The pathophysiology ofDVT comes froma triangle of possible changes in the venous system.The triad consists ofchanges in the vessel wall, changes in thepattern of blood flow and changes in the constituency of the blood.These changes can occur as a result of pathology, therapies andtreatments. Injuryin the vessel wall may result from trauma,surgery or rather invasive treatments.

DVTnormally occurs when there is a clotting of the blood in a deep veinof an extremity or the pelvis. DVT isthe primary cause of pulmonary embolism and it results from the conditions thatimpair venous return, lead to endothelial dysfunction or lead to hyper coagulability. DVT can cause pain and swelling in anextremity. When DVT is suspected a dimmer testing is used .Thetest is very important since a negative result helps to exclude DVT whereas a positive result is not specific and requires additional testing to confirm DVT. Anticoagulants are used for thetreatment of DVT once it has been confirmed positive.

Similaritiesand differences between CVI and DVT

DVTcommonly occurs in the lower extremities or the pelvis. Long termcomplications of DVT are such as venous insufficiency with or withoutpost phlebitic syndrome. Lower extremity DVT is more likely to causepulmonary embolism because of higher clot burden. There are manyfactors that contribute to DVT. These factors are such as cancerparticularly in elder patients as well as in patients with recurrentthrombosis. DVT may result to various complications such as chronicvenous insufficiency, postphlebitic syndrome and pulmonary embolism.Acute DVT normally lead s to phlegmasia alba dolens or phlegmasiacerulean dolens which can result to venous gangrene if not promptlydiagnosed and treated (Rooke et al 2007).

DVTmay occur in ambulatory patients or as a complication of surgery.Among the high risk hospitalized patients, most deep vein thrombi occur in the small calf veins and may not be detected. Thedifference between physiology of CVI and DVT is that DVTis a clotin the deep veins of the legs.DVT can lead to pieces of the clotbreaking off and going to the lungs and this is normally referred toas pulmonary embolism.

Onthe other hand, CVI is associated with the superficial veins. It occurs when the valves in the veins do not work and blood can flow backwards in the veins. CVI consists of symptoms such aspain, swellings and others. The similarity between CVI and DVT isthat CVI often results after suffering DVT. Even if the blood clot is cleared out by the body’s natural defenses ,the venous valves in most cases become stuck to the wall of the veins and nolonger prevent blood flow from travelling backward with gravity towards the legs and feet. Chronic venous insufficiency (CVI)represents an important medical and social problem with a significantimpact on the quality of life.

Geneticfactor and its Pathophysiology Impact of CVI and DVT

Althoughthe mechanisms of occurrence and development of chronic venousinsufficiency became better understood in the last decades, thecontribution of genetic risk factors is not precisely established.Many factors are involved in the etiopathogenesis of CVI, such asage, sex, heredity, sedentary life style. The impact of geneticfactors is variably estimated. Gene’s polymorphisms associated withhyperhomocysteinemia, coagulation abnormalities, genetic factorsinvolved in venous thrombosis leading to secondary CVI, represent thegenetic background of these complex diseases.

Inconclusion, other the risk factors most closely associated with CVIwere age, family history of varicose veins, and constipation,whatever the sex. This is in keeping with findings from recentepidemiologic studies. Obesity and lack of physical activity werestrongly associated with CVI in women, more so than in men. Thenumber of pregnancies (more than 2 pregnancies) significantlydistinguished between women with and without CVI, (Ballard, &ampBergan 2000).

Reviewthe Mind Maps-Dementia, Gastro,Gerd. Construct the Mind Map of Dvtand Cvi Consider the Epidomology and Clinica

Amind map is a powerful graphic technique that provides a key tounlock potential of the brain. Cortical skills are harnessed, forinstance words, images, logic, rhythm and spatial awareness. HubaBolero says that mind mapping can be to every aspect of life whereleaning and thinking is clearer and improved. However, some peoplebelieve that we should be educated enough because health care personsare just that primary care and move you out to treat the next one.The system seems to be overloaded and that we should all share ideasso that not many people would go untreated.

Amind Map of CVI and DVT

Therapiesthat are adjunctive to improve oxygenation and ventilation propertiesof NO clinical trials of NO- Numerous clinical observational studieshave demonstrated improvements in oxygenation by improving VQmismatch as demonstrated by a 10% to 20% increase in PaO2/FIO2 ratioand a reduction on pulmonary vascular resistance and mean pulmonaryarterial pressures by atleast 5 to 8 mm Hg.

Clinicaluse of nitric-oxide- Given that doses below 40 ppm were safe withoutany significant adverse effects, it can be considered a &quotrescue&quottherapy to possibly allow for more protective forms of ventilationwith decreases in FIO2 and mean airway pressures to maintainacceptable oxygenation or in situations in which secondary pulmonaryhypertension leads to compromised hemodynamic function from rightventricular failure potential indications include:

InhaledNO is typically started at low doses ranging from 1 to 2 ppm andgradually increased until the desired effect is achieved. Consensusconference on NO use, is to perform a dose response test starting at20 ppm and reducing the doses to 10, 5, and 0 ppm to find the lowesteffective dose. A significant response should be considered as a 20%increase in the PaO2/FIO2 ratio or at least a 5mm Hg decrease in themean pulmonary artery pressure. – The improvement in gas exchange isusually seen at lower doses. The dose required to reduce meanpulmonary artery pressure is usually higher. The usual dose rangesfrom 10 to 40 ppm. – Doses greater than 80 ppm are associated with ahigher risk for adverse effects. Adverse effects of nitricoxideinclude

(i)the formation of methemoglobin and

(ii)the spontaneous oxidation to nitrogen dioxide (NO2). NO2 is known tobe toxic to the

respiratorysystem with maximal exposure limited to 5 ppm. Complications from NO2exposure include airway irritation and hyperreactivity with levels aslow as 1.5 ppm, pulmonary edema, and pulmonary fibrosis when exposedto higher levels.

(iii)Rebound pulmonary: vasoconstriction can occur with suddendiscontinuation leading to rapid worsening of VQ mismatch andpulmonary hypertension with significant hemodynamic collapse safeadministration of nitric oxide.

Clinicalsituations in which heliox may be used include conditions with highairflow resistance such as severe acute exacerbations of asthmaorCOPD, bronchiolitis,

bronchopulmonarydysplasia, and extrathoracic or tracheal obstruction. – Disadvantagesof using heliox in critically ill patients include the cost oftherapy and the high concentrations of helium required. Most studiesutilize helium: oxygen mixes of 80:20 or 70:30 to achieve atherapeutic benefit. At higher concentrations of oxygen, the effectof helium is less and therefore is limited in use to those notrequiring high FIO2. Ventilators also require recalibration formeasured FIO2, flows, and tidal volumes when using heliox


Ballard,J. L., &amp Bergan, J. J. (2000).ChronicVenous Insufficiency: Diagnosis and Treatment.London: Springer London.

Huether,S. E., &amp McCance, K. L. (2012). Understanding pathophysiology(Laureate custom ed.). St. Louis, MO: Mosby.

Chapter22, “Structure and Function of the Cardiovascular and LymphaticSystems”

McPhee,S. J., &amp Hammer, G. D. (2012). Pathophysiology of disease: Anintroduction to clinical medicine (Laureate Education, Inc., customed.). New York, NY: McGraw-Hill Medical.

Rooke,T. W., Sullivan, T. M., Jaff, M. R., &amp Society for VascularMedicine and Biology. (2007). Vascularmedicine and endovascular interventions.Malden, MA: Blackwell Futura.

Valji,K., &amp Valji, K. (2012).Thepractice of interventional radiology: With online cases and videos.Philadelphia, PA: Elsevier/Saunders.