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ALTERATIONS OF CARDIOVASCULAR FUNCTION EUGENE PARDI, DO MARICOPA COMMUNITY COLLEGES ESTRELLA MOUNTAIN COMMUNITY COLLEGE DISEASES OF THE VEINS: VARICOSE VEINS & CHRONIC VENOUS INSUFFICIENCY ▪ VARICOSE VEIN: a vein in which blood has pooled, producing distended, tortuous, and palpable vessels. ▪ Caused by: ▪ Trauma to the saphenous veins that damages one or more valves. ▪ Gradual venous distention caused by the action of gravity on blood in the legs. EUGENE PARDI, DO 10/4/2013 2 EUGENE PARDI, DO 10/4/2013 3 DISEASES OF THE VEINS: VARICOSE VEINS & CHRONIC VENOUS INSUFFICIENCY ▪ If a valve is damaged, a section of the vein is subjected to the pressure of a larger volume of blood under the influence of gravity. ▪ The vein swells as it becomes engorged with blood. ▪ Surrounding tissue becomes edematous as increased hydrostatic pressure pushes plasma through the stretched vessel wall. ▪ Venous distention develops over time in individuals who stand for long periods, wear constricting garments, or cross the legs at the knees. ▪ Diminishes the action of the muscle pump. EUGENE PARDI, DO 10/4/2013 4 EUGENE PARDI, DO 10/4/2013 5 EUGENE PARDI, DO 10/4/2013 6 DISEASES OF THE VEINS: VARICOSE VEINS & CHRONIC VENOUS INSUFFICIENCY ▪ Risk factors include: ▪ Age ▪ Female gender. ▪ Family history of varicose veins. ▪ Obesity. ▪ Pregnancy. ▪ Deep venous thrombosis. ▪ Previous leg injury ▪ The increased pressure in the vein damages venous valves, rendering them incompetent and unable to maintain normal venous pressure. EUGENE PARDI, DO 10/4/2013 7 DISEASES OF THE VEINS: VARICOSE VEINS & CHRONIC VENOUS INSUFFICIENCY ▪ Varicose veins and valvular incompetence can progress to CHRONIC VENOUS INSUFFICIENCY (CVI). ▪ CVI is inadequate venous return over a long period. ▪ Venous hypertension, circulatory stasis, and tissue hypoxia cause an inflammatory reaction in vessels and tissue leading to fibrosclerotic remodeling of the skin and then to ulceration. ▪ Symptoms: edema of the lower extremities which may extend to the knee and hyperpigmentation of the skin of the feet and ankles. EUGENE PARDI, DO 10/4/2013 8 EUGENE PARDI, DO 10/4/2013 9 DISEASES OF THE VEINS: VARICOSE VEINS & CHRONIC VENOUS INSUFFICIENCY ▪ Circulation to the extremities can become so sluggish that the metabolic demands of the cells are barely met. ▪ Any trauma or pressure can lower the O2 supply and cause cell death and necrosis (VENOUS STASIS ULCERS). ▪ Infection can occur due to the sluggish circulation. ▪Infection following reparative surgery is a significant risk. EUGENE PARDI, DO 10/4/2013 10 EUGENE PARDI, DO 10/4/2013 11 DISEASES OF THE VEINS: VARICOSE VEINS & CHRONIC VENOUS INSUFFICIENCY ▪ Treatment of varicose veins and CVI: ▪ Elevating the legs. ▪ Wearing compression stockings. ▪ Physical exercise. ▪ Sclerotherapy or surgical ligation. ▪ Conservative vein resection. ▪ Vein stripping. EUGENE PARDI, DO 10/4/2013 12 Before Vein Ablation, photo courtesy of Dr. Robert Min After Vein Ablation, photo courtesy of Dr. Robert Min EUGENE PARDI, DO 10/4/2013 13 Treatment: Support Stockings Treatment: Sclerotherapy EUGENE PARDI, DO Treatment: Laser Therapy Sclerotherapy: Before and After Treatment: Vein Surgery Treatment: Endovenous Laser 10/4/2013 14 EUGENE PARDI, DO 10/4/2013 15 DISEASES OF THE VEINS: THROMBUS FORMATION IN VEINS ▪THROMBUS: a blood clot that remains attached to a vessel wall. ▪THROMBOEMBOLUS: a detached thrombus. ▪Venous thrombi are more common than arterial thrombi because flow and pressure are lower in the veins than in the arteries. EUGENE PARDI, DO 10/4/2013 16 EUGENE PARDI, DO 10/4/2013 17 DISEASES OF THE VEINS: THROMBUS FORMATION IN VEINS ▪ DEEP VENOUS THROMBOSIS (DVT): occurs primarily in the lower extremity. ▪ The TRIAD OF VIRCHOW are three factors that promote venous thrombosis. ▪Venous stasis (e.g. immobility, age, CHF). ▪Venous endothelial damage (e.g. trauma, intravenous medications). ▪Hypercoagulable states (e.g. inherited disorders, malignancy, pregnancy, use of oral contraceptives, or HRT). EUGENE PARDI, DO 10/4/2013 18 EUGENE PARDI, DO 10/4/2013 19 Contributions from cells, plasma, and blood flow (Virchow's Triad) regulate fibrin formation and therefore, fibrin network structure and stability. EUGENE PARDI, DO 10/4/2013 20 DISEASES OF THE VEINS: THROMBUS FORMATION IN VEINS ▪ Accumulation of clotting factors and platelets leads to thrombus formation in the vein, often near a venous valve. ▪ Inflammation promotes further platelet aggregation, and the thrombus propagates or grows proximally. ▪ If the vein is deep in the leg, the inflammation is not accompanied by clinical symptoms or signs. ▪ If the thrombus creates obstruction to venous blood flow, edema of the leg may occur. EUGENE PARDI, DO 10/4/2013 21 EUGENE PARDI, DO 10/4/2013 22 EUGENE PARDI, DO 10/4/2013 23 DISEASES OF THE VEINS: THROMBUS FORMATION IN VEINS ▪ THROMBUS FORMATION (CONT’D): ▪ Most thrombi eventually dissolve without treatment. ▪ Untreated DVT is associated with a high risk of PULMONARY EMBOLISM. ▪ Persistent venous obstruction may lead to chronic venous insufficiency and post – thrombotic syndrome with associated pain, edema, and ulceration of the affected limb. EUGENE PARDI, DO 10/4/2013 24 EUGENE PARDI, DO 10/4/2013 25 EUGENE PARDI, DO 10/4/2013 26 DISEASES OF THE VEINS: THROMBUS FORMATION IN VEINS ▪ Prevention of DVT in at – risk individuals is important and includes early ambulation, pneumatic devices, and prophylactic anticoagulation. ▪ If thrombosis does occur, diagnosis is confirmed by a combination serum D – dimer measurement and Doppler ultrasonography. ▪ Management consists of anticoagulation therapy with heparin and warfarin. ▪ In selected individuals, thrombolytic therapy or placement of an inferior vena cava filter may be indicated. EUGENE PARDI, DO 10/4/2013 27 EUGENE PARDI, DO 10/4/2013 28 DISEASES OF THE VEINS: SUPERIOR VENA CAVA SYNDROME ▪ A progressive occlusion of the superior vena cava (SVC) that leads to venous distention in the upper extremities and head. ▪ Causes: ▪ Bronchogenic cancer (75% of cases). ▪ Lymphomas. ▪ Metastasis of other cancers. ▪ Tuberculosis. ▪ Mediastinal fibrosis. ▪ Cystic fibrosis ▪ Invasive therapies (pacemaker wires, central venous catheters, and pulmonary artery catheters). EUGENE PARDI, DO 10/4/2013 29 DISEASES OF THE VEINS: SUPERIOR VENA CAVA SYNDROME ▪ The SVC is a low pressure vessel that lies in the thoracic compartment of the mediastinum. ▪ The right main stem bronchus abuts the SVC so that cancers occurring in this bronchus may exert pressure on the SVC. ▪ The SVC is surrounded by lymph nodes and lymph chains that frequently become involved in thoracic cancers and compress the SVC during tumor growth. ▪ Onset of SVCS is slow, so collateral venous drainage to the azygos vein usually has time to develop. EUGENE PARDI, DO 10/4/2013 30 EUGENE PARDI, DO 10/4/2013 31 DISEASES OF THE VEINS: SUPERIOR VENA CAVA SYNDROME ▪ CLINICAL MANIFESTATIONS: are edema and venous distention in the upper extremities and face. ▪ Patients complain of a feeling of fullness in the head or tightness of shirt collars, necklaces, and rings. ▪ Cerebral edema can cause headache, visual disturbance, and impaired consciousness. ▪ Skin of the face and arms may become cyanotic and taut. ▪ Capillary refill time is prolonged. ▪ Respiratory distress may be present because of edema of bronchial structures or compression of the bronchus by a carcinoma. EUGENE PARDI, DO 10/4/2013 32 DISEASES OF THE VEINS: SUPERIOR VENA CAVA SYNDROME ▪ DIAGNOSIS: made by CXR, Doppler studies, CT, MRI, and ultrasound. ▪ Not a vascular emergency due to its slow onset and development of collateral venous drainage. ▪ Considered an oncologic emergency if the cause is from a cancer. EUGENE PARDI, DO 10/4/2013 33 EUGENE PARDI, DO 10/4/2013 34 DISEASES OF THE VEINS: SUPERIOR VENA CAVA SYNDROME ▪ TREATMENT: for malignant disorders can include radiation therapy, surgery, chemotherapy, and the administration of diuretics, steroids, and anticoagulants. ▪ Treatment for nonmalignant causes may include bypass surgery using various grafts, thrombolysis (both locally and systemically), balloon angioplasty, and placement of intravascular stents. EUGENE PARDI, DO 10/4/2013 35 A and B show orthogonal venograms in a 36-year-old woman with a history of acute promyelocytic leukemia who had undergone treatment with chemotherapy via an indwelling subclavian catheter. Fifteen months previously, following courses of chemotherapy, she had developed SVC syndrome and had balloon dilatation alone of the caval-atrial junction. At this study, she presented with recurrent SVC syndrome and there is restenosis at the site of the prior venoplasty (arrows). EUGENE PARDI, DO The lesion in Figure 1 has been crossed with a guidewire and initial dilatation performed (A) with a 12 mm × 40 mm XXL balloon (Meditech-Boston Scientific). Following balloon dilatation, there was evidence of elastic recoil and a Palmaz 308 stent was positioned across the residual lesion (B). The small arrows indicate the proximal and distal ends of the stent. Stent deployment was performed (C), covering the lesion (arrow). After postdilatation, the expanded stent can be seen in place and a pressure gradient was measured (A). Wide patency is documented with venography 10/4/2013 36 DISEASES OF THE ARTERIES: HYPERTENSION ▪ HYPERTENSION (HTN) is consistent elevation of systemic arterial blood pressure. ▪ The most common primary diagnosis in the United States. ▪ One in three Americans has hypertension. ▪ > 2/3 of those older than 60 are affected. ▪ The chance of developing primary HTN increases with age. ▪ HTN does occur in children & is being diagnosed with increasing frequency. EUGENE PARDI, DO 10/4/2013 37 DISEASES OF THE ARTERIES: HYPERTENSION ▪ HTN is defined as a sustained systolic blood pressure of 140 mm Hg or greater or a diastolic pressure of 90 mm Hg or greater. ▪ All stages of HTN are associated with increased risk for target organ disease events. ▪ MI, kidney disease, and stroke. ▪ Both stage I and stage II HTN need effective long – term therapy. EUGENE PARDI, DO 10/4/2013 38 EUGENE PARDI, DO 10/4/2013 39 EUGENE PARDI, DO 10/4/2013 40 DISEASES OF THE ARTERIES: HYPERTENSION ▪ ISOLATED SYSTOLIC HYPERTENSION (ISH) defined as a sustained systolic blood pressure (BP) that is ≥140 mm Hg and a diastolic measurement that is < 90 mm Hg. ▪ ISH is strongly associated with cardiovascular and cerebrovascular events. ▪ Most cases of HTN are diagnosed as PRIMARY HYPERTENSION (also called ESSENTIAL or IDIOPATHIC HYPERTENSION). ▪ 92% to 95% of hypertensive individuals have primary disease. ▪ SECONDARY HYPERTENSION is caused by an underlying disorder, such as renal disease. EUGENE PARDI, DO 10/4/2013 41 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HYPERTENSION: a combination of genetic and environmental factors is responsible for its development. ▪ Genetic predisposition to HTN is believed to be polygenic. ▪ Factors associated with primary HTN include: ▪ Family history of HTN. ▪ Advancing age. ▪ Gender (men younger than age 55; women after age 70). ▪ Black race. ▪ High dietary sodium intake. EUGENE PARDI, DO 10/4/2013 42 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ Factors associated with primary HTN (cont’d): ▪Glucose intolerance (insulin resistance and diabetes mellitus). ▪Cigarette smoking. ▪Obesity. ▪Heavy alcohol consumption. ▪Low dietary intake of potassium, calcium, and magnesium. EUGENE PARDI, DO 10/4/2013 43 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ Many of these factors are also risk factors for other cardiovascular disorders. ▪Obesity, hypertension, dyslipidemia, and glucose intolerance are found together in a condition called the METABOLIC SYNDROME. EUGENE PARDI, DO 10/4/2013 44 EUGENE PARDI, DO 10/4/2013 45 EUGENE PARDI, DO 10/4/2013 46 DISEASES OF THE ARTERIES: HYPERTENSION ▪PRIMARY HTN (CONT’D): ▪PATHOPHYSIOLOGY: ▪Hypertension results from a sustained increase in peripheral resistance (arteriolar vasoconstriction), an increase in circulating blood volume, or both. EUGENE PARDI, DO 10/4/2013 47 DISEASES OF THE ARTERIES: HYPERTENSION •Primary HTN is the result of an interaction of genetics and the environment. •Multiple pathophysiologic mechanisms mediate this interaction. •The SNS, the renin – angiotensisn – aldosterone system (RAAS), and the natriuretic peptides. PRIMARY HTN •Inflammation, endothelial dysfunction, (CONT’D): obesity – related hormones, and insulin resistance contribute to both increased peripheral resistance and increased blood volume. EUGENE PARDI, DO 10/4/2013 48 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ Increased volume is related to a shift in the PRESSURE – NATRIURESIS RELATIONSHIP. ▪For a given blood pressure, individuals with HTN tend to secrete less salt in their urine. ▪ The SNS has been implicated in both the development and the maintenance of elevated blood pressure. ▪Also plays a role in hypertensive end organ damage. EUGENE PARDI, DO 10/4/2013 49 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ Overactivity of the RAAS contributes to salt and water retention and increased vascular resistance. ▪ High levels of angiotensin II contributes to endothelial dysfunction, insulin resistance, and platelet aggregation. ▪ Angiotensin II mediates structural change in the vessel wall resulting in permanent increases in peripheral resistance. ▪ Angiotensin II is associated with end – organ effects of HTN ▪ Atherosclerosis. ▪ Renal disease. ▪ Cardiac hypertrophy. EUGENE PARDI, DO 10/4/2013 50 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ Overactivity of the RAAS (CONT’D): ▪ Aldosterone contributes to sodium retention by the kidney and has other deleterious effects on the cardiovascular system. ▪ ANGIOTENSIN – CONVERTING ENZYME (ACE) INHIBITORS and ANGIOTENSIN RECEPTOR BLOCKERS (ARBs) oppose the activity of the RAAS and are effective in reducing blood pressure and protecting against target organ damage. EUGENE PARDI, DO 10/4/2013 51 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ The natriuretic hormones modulate renal sodium (Na+) excretion and require adequate K+, Ca++, and Mg++ to function properly. ▪Atrial natriuretic peptide (ANP) ▪Brain natriuretic peptide (BNP) ▪C – type natriuretic peptide (CNP) ▪Urodilantin EUGENE PARDI, DO 10/4/2013 52 EUGENE PARDI, DO 10/4/2013 53 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ In HTN, increased ANP and BNP levels are linked to an increased risk for ventricular hypertrophy, atherosclerosis, and heart failure. ▪ Salt retention leads to water retention and increased blood volume, which leads to an increase in blood pressure. EUGENE PARDI, DO 10/4/2013 54 EUGENE PARDI, DO 10/4/2013 55 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ Inflammation plays a role in the pathogenesis of HTN. ▪Chronic inflammation contributes to vascular remodeling and smooth muscle contraction. ▪Endothelial injury and dysfunction leads to a decreased production of vasodilators, NO2, and an increased production of vasoconstrictors, endothelin. EUGENE PARDI, DO 10/4/2013 56 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ Obesity is a risk factor for HTN in both adults and children. ▪Causes changes in the ADIPOKINES (LEPTIN and ADIPONECTIN) and is associated with increased activity of the SNS and the RAAS. ▪Is linked to inflammation, endothelial dysfunction, and insulin resistance and an increased risk for cardiovascular complications from HTN. EUGENE PARDI, DO 10/4/2013 57 DISEASES OF THE ARTERIES: HYPERTENSION ▪ PRIMARY HTN (CONT’D): ▪ Insulin resistance is common in HTN, even in individuals without clinical diabetes. ▪ Associated with decreased endothelial release of NO2 and other vasodilators. ▪ Insulin resistance also causes renal salt and water retention. ▪ Is associated with Overactivity of the SNS and the RAAS. ▪ The interactions between obesity, HTN, insulin resistance, and lipid disorders in the METABOLIC SYNDROME result in a high risk of cardiovascular disease. EUGENE PARDI, DO 10/4/2013 58 DISEASES OF THE ARTERIES: HYPERTENSION ▪ SECONDARY HYPERTENSION: caused by an underlying disease process or medication that raises peripheral vascular resistance or cardiac output. ▪ Renal vascular or parenchymal disease. ▪ Adrenocortical tumors. ▪ Adrenomedullary tumors (pheochromocytoma). ▪ Drugs (OCPs, corticosteroids, antihistamines). ▪ If the cause is removed or the drug discontinued before permanent structural change occurs, BP will return to normal. EUGENE PARDI, DO 10/4/2013 59 DISEASES OF THE ARTERIES: HYPERTENSION ▪ COMPLICATED HYPERTENSION: when the HTN becomes more severe and chronic, tissue damage can occur in the blood vessels and tissues, leading to target organ damage in the heart, kidney, brain, and eyes. ▪ CV complications include left ventricular hypertrophy, angina pectoris, heart failure, coronary artery disease, MI, and sudden death. ▪ Vascular complications include the formation, dissection, and rupture of aneurysms and atherosclerosis leading to vessel occlusion. EUGENE PARDI, DO 10/4/2013 60 DISEASES OF THE ARTERIES: HYPERTENSION ▪ COMPLICATED HYPERTENSION (CONT’D): ▪ Renal complications include parenchymal damage, nephrosclerosis, renal arteriosclerosis, and renal insufficiency or failure. ▪MICROALBUMINURIA is an early sign of impending renal dysfunction and significantly increased risk for CV events, especially in those who have DM. EUGENE PARDI, DO 10/4/2013 61 DISEASES OF THE ARTERIES: HYPERTENSION ▪COMPLICATED HYPERTENSION (CONT’D): ▪Complications specific to the retina include retinal vascular sclerosis, exudation, and hemorrhage. ▪Cerebrovascular complications include TIA’s, stroke, cerebral thrombosis, aneurysm, hemorrhage, and dementia. EUGENE PARDI, DO 10/4/2013 62 DISEASES OF THE ARTERIES: HYPERTENSION ▪ MALIGNANT HYPERTENSION: rapidly progressive hypertension in which DIASTOLIC pressure is greater than 140 mm Hg (normal < 90 mm Hg). ▪ High arterial pressure renders the cerebral arterioles incapable of regulating blood flow to the cerebral capillary beds. ▪ Due to the high pressure, capillaries exude fluid into the interstitial space. ▪ Cerebral edema and cerebral dysfunction (ENCEPHALOPATHY) occurs and increases until death if the HTN is not reduced. ▪ Organ damage from malignant HTN is life threatening. ▪ Malignant HTN can also cause papilledema, cardiac failure, uremia, retinopathy, and CVA. EUGENE PARDI, DO 10/4/2013 63 DISEASES OF THE ARTERIES: HYPERTENSION ▪ CLINICAL MANIFESTATIONS: the early stages of HTN have no clinical manifestations other than elevated blood pressure. ▪ HTN is called a “silent disease”. ▪ If HTN is not detected or treated, it becomes established and may begin to accelerate its effects on tissues when the individual is 30 to 50 years of age. ▪ Complications of HTN begin to appear during the fourth, fifth, and sixth decades of life EUGENE PARDI, DO 10/4/2013 64 DISEASES OF THE ARTERIES: HYPERTENSION ▪ CLINICAL MANIFESTATIONS (CONT’D): ▪ Most clinical manifestations of hypertensive disease are caused by complications that damage organs and tissues outside the vascular system. ▪ Signs and symptoms are specific for the organs or tissues affected. ▪ Heart disease, renal insufficiency, CNS dysfunction, impaired vision, impair mobility, vascular occlusion, or edema can all be caused by sustained HTN. EUGENE PARDI, DO 10/4/2013 65 DISEASES OF THE ARTERIES: HYPERTENSION ▪ EVALUATION AND TREATMENT: diagnosis requires the measurement of blood pressure on at least two separate occasions, averaging two readings at least 2 minutes apart, with the following conditions: ▪ The person is seated, the arm is supported at heart level, the person must be at rest for at least 5 minutes, and the person should not have smoked or ingested any caffeine in the previous 30 minutes. ▪ Diagnostic tests for a complete evaluation of HTN include: ▪ 24 – hour blood pressure monitoring in selected individuals. ▪ CBC, UA, biochemical blood profile (plasma glucose, sodium, potassium, calcium, magnesium, creatinine, cholesterol with fractions, and triglycerides). ▪ Electrocardiogram (ECG). EUGENE PARDI, DO 10/4/2013 66 DISEASES OF THE ARTERIES: HYPERTENSION ▪ EVALUATION AND TREATMENT (CONT’D): ▪ If the initial diagnostic screening is negative for any underlying disease, then the patient has essential or primary HTN. ▪ Treatment of primary HTN depends on its severity. ▪ Life style modification is important for prevention of HTN and as part of a treatment regimen. ▪ Modifications include an exercise program, dietary modifications, stopping smoking, and losing weight. EUGENE PARDI, DO 10/4/2013 67 DISEASES OF THE ARTERIES: HYPERTENSION ▪ EVALUATION AND TREATMENT (CONT’D): ▪ Pharmacologic treatment of HTN reduces the risk of end – organ damage and prevents major diseases (MI and CVA). ▪Diuretics have been effective in lowering BP and preventing cardiovascular complications. ▪An ACE inhibitor, ARB, or aldosterone antagonist might be effective in the patients in heart failure, chronic kidney disease, or who have a history of MI and stroke. EUGENE PARDI, DO 10/4/2013 68 DISEASES OF THE ARTERIES: HYPERTENSION ▪ EVALUATION AND TREATMENT (CONT’D): ▪ Pharmacologic treatment (cont’d): ▪Some patients require two or more drugs for BP control, including combinations of diuretics and other antihypertensives, such as beta blockers, calcium channel blockers, and ACE inhibitors. ▪Careful follow – up to support continued adherence, determine the response, and monitor for side effects of these medications is important. EUGENE PARDI, DO 10/4/2013 69 DISEASES OF THE ARTERIES: HYPERTENSION EUGENE PARDI, DO 10/4/2013 70 DISEASES OF THE ARTERIES: HYPERTENSION EUGENE PARDI, DO 10/4/2013 71