amol gulhane -peripheral vascular disease

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  1. 1. Dr amol gulhane DNB resident CARE hospitals , hyd
  2. 2. inner layer of endothelium (intima) middle layer of connective tissue, smooth muscle and elastic fibers (media) outer layer of connective tissue (adventitia) have smooth muscles that contracts & relaxes to respond changes in blood volume.
  3. 3. charac. by a reduction in blood flow and hence 02 through the peripheral vessels when the need of the tissues for 02 exceeds the supply, areas of ischemia and necrosis will develop Factors that can contribute to the development of peripheral vascular disorders : atherosclerotic changes thrombus formation embolization coagulability of blood hypertension inflammatory process/infection
  4. 4. Atherosclerosis Thrombosis or embolism Aneurysm Intimal dissection Pseudo-aneurysm Arterio-venous fistula Arteritis Entrapment syndrome Cystic adventitial disease Most common cause
  5. 5. Arterial Insufficiency there is a deceased blood flow toward the tissues, producing ischemia pulses are usually diminished or absent sharp, stabbing pain occurs because of the ischemia, particularly with activity ischemic ulcers and changes in the skin.
  6. 6. 1. Age (elderly) blood vessels become less elastic, become thin walled and calcified PVR BP 2. Sex (male) 3. Cigarette smoking nicotine causes vasoconstriction and spasm of the arteries circulation to the extremities C02 inhaled in cigarette smoke reduces 02 transport to tissues 4. Hypertension cause elastic tissues to be replaced by fibrous collagen tissue arterial wall become less distensible resistance to blood flow BP 5. Hyperlipedimia atherosclerotic plaque 6. Obesity places added burden on the heart & blood vessels excess fat contribute to venous congestion
  7. 7. 7. Lack of physical activity Physical activity promotes muscle contraction venous return to the heart aids in development of collateral circulation 8. Emotional stress stimulates sympathetic N.S. - peripheral vasoconstriction BP 9. Diabetes mellitus changes in glucose & fat metabolism promote the atherosclerotic process 10. Family history of arthrosclerosis
  8. 8. is a disorder in which there is an arteriosclerotic narrowing or obstruction of the inner & middle layer of the artery most common cause of arterial obstructive disease in the extremities the lower extremities are involved more than upper extremities common site of disease femoral artery, iliac arteries, popliteal arteries in a diabetic, the disease becomes more progressive, affects the smaller arteries and often involves vessels below the knee
  9. 9. Sub-diaphragmatic aorta 21 24 mm Infra-diaphragmatic aorta 17 20 mm Common iliac artery 10 12 mm External iliac artery 8 10 mm Common femoral artery 7 9 mm Superficial femoral artery 6 8 mm Popliteal artery 4 6 mm
  10. 10. Plaque formation on the intimal wall that causes partial or complete occlusion Calcification of the medial layer and a gradual loss of elasticity weakens the arterial walls predisposes to aneurysm, dilation or thrombus formation artery is unable to transport an adequate blood volume to the tissues during exercise or rest
  11. 11. Intermittent claudication most common pain during exercise disappear w/in 1-2 mins. after stopping the exercise or resting the femoral artery is often affected pain in the calf muscle common symptom pain at rest is indicative of severe disease In advanced arteriosclerosis obliterans ischemia may lead to necrosis, ulceration and gangrene toes and distal foot
  12. 12. Stage Complains I Asymptomatic II a II b Mild claudication Moderate to severe claudication III Ishemic rest pain IV Ulcer or gangrene Clinical classification The Rutherford classification
  13. 13. TASC II classication of femoral and popliteal lesions type A lesions single stenosis 10 cm in length single occlusion 5 cm in length type B lesions multiple lesions (stenoses or occlusions), each 5 cm single stenosis or occlusion 15 cm not involving the infrageniculate popliteal artery type C lesions multiple stenoses or occlusions totaling > 15 cm with or without heavy calcification recurrent stenoses or occlusions that need treatment after two endovascular interventions type D lesions chronic total occlusion of the common or superficial femoral artery (> 20 cm, involving the popliteal artery)chronic total occlusion of the popliteal artery and proximal trifurcation vessels
  14. 14. Doppler ultrasonography audible tone produced in proportion to blood velocity measure blood flow through vessels
  15. 15. Ankle brachial Pressure The systolic pressure at any level of the lower extremity can be measured by positioning a pneumatic cuff at the desired site. Any patent artery distal to the cuff that is accessible to Doppler ultrasound can be used for flow detection, but the posterior tibial (PT) and dorsalis pedis (DP) arteries are usually most convenient. When the cuff is inflated to above systolic pressure, the arterial flow signal disappears. As cuff pressure is gradually lowered to slightly below systolic pressure, the flow signal reappears, and the pressure at which flow resumes is recorded as the systolic pressure
  16. 16. In general, measurement of ankle systolic pressure is the most valuable physiologic test for assessing the arterial circulation in the lower limb. If the pressure measured by a cuff placed just above the malleoli is less than that of the upper arm, proximal occlusive disease in the arteries to the lower limb is invariably present. The ratio of ankle systolic pressure to brachial systolic pressure is called the ankle-brachial index or ABI.
  17. 17. In the absence of proximal arterial occlusive disease, the ankle-brachial index is greater than 1 .0, (mean value of 1 . 1 1 0.10) values greater than 0.90 are typically interpreted as normal. Usually limbs with single-level occlusions have indexes greater than 0.5, and limbs with lesions at multiple levels have indexes less than 0.5 Many limbs with impending gangrene or ischemic ulceration have absent Doppler flow signals at the ankle level.
  18. 18. ABPI Comment > 1.3 Falsely high value (suspicion of medial sclerosis) 0.9 1.3 Normal finding0.75 0.9 Mild PAD 0.4 0.75 Moderate PAD < 0.4 Severe PAD
  19. 19. Calcification of vessel walls Beaded appearance of color flow Ankle pressure 280 mmHg Brachial pressure 120 mmHg ABPI 2.3 Falsely elevated recordings in diabetic patients Calcified & rigid arterial walls
  20. 20. Narrow frequency band Steep systolic increase Quick drop Early diastolic reverse flow ( of systolic flow amplitude) Late diastolic short forward flow
  21. 21. Cardiac pump function Cardiac insufficiency Aortic valve function Aortic stenosis/insufficiency Course of vessel Tortuosity Vessel branching Peripheral vascular resistance Peripheral inflammation Polyneuropathy Warm or cold extremity Vaso-spastic disorders
  22. 22. Hyperemic (normal PSV& normal RT*) Exercise Fever Downstream infection Temporary arterial occlusion by blood pressure cuff Tardus-Parvus waveform (low PSV & longer RT) Distal to severe stenosis or occlusion * Rise time: Time between beginning of systole & peak systole
  23. 23. Normal triphasic waveform Normal DPA at rest Monophasic hyperemic flow Following exercise
  24. 24. Monophasic waveform Normal PSV Normal rise time
  25. 25. Proximal to stenosis The character of Doppler signals obtained proximal to an arterial obstruction depends on the capability of the collateral circulation. If there are wel ldeveloped collaterals between the Doppler probe and the point of obstruction, the waveform may be relatively normal.
  26. 26. If the Doppler probe is placed directly over a stenotic lesion, the signal has an abnormally high peak systolic frequency. This reflects the increased flow velocity in the stenotic segment. At site of stenosis
  27. 27. When a waveform is obtained from an arterial site distal to a stenosis or occlusion, a single, forward velocity component is observed, with flow remaining above the zero baseline throughout the cardiac cycle. The peak systolic frequency is lower than normal, and the waveform becomes flat and rounded Distal to stenosis
  28. 28. High resistance, low volume waveform Characteristic shoulder on systolic downstroke Due to pulse wave reflection from distal disease ShoulderShoulder
  29. 29. Tardus: Longer rise time Parvus: Low PSV Severe stenosis or occlusion Tardus-Parvus waveformDamping waveform Increased systolic rise time Loss of pulsatility
  30. 30. IF superficial femoral artery is patent, a PI less than 4 indicates a hemodynamically significant aortoiliac lesion, The PI of the normal common femoral artery has a mean value of 6.7. More distally, the PI increases to 8 in the popliteal and 14 in the PT artery A PI value greater than or equal to 4 is predictive of a hemodynamically normal aortoiliac segment.
  31. 31. Aorto-iliac: 25 % Femoro-popliteal: 65% Infra-popliteal: 10%
  32. 32. Proximal: 2 cm proximal to stenosis At stenosis : Same Doppler angle if possible
  33. 33. Vr= psv ratio
  34. 34. SFA: PSV of A 69 cm/sec PSV of B 349 cm/sec B / A 349 / 69 = 5 > 80% diameter stenosis
  35. 35. 2 severe stenoses demonstrated in SFA Areas of color flow disturbance & aliasing (arrows)
  36. 36. Drop-out of color flow signal in parts of lumen
  37. 37. Occlusion in CIA Reversed flow in IIA (blue) to supply flow to EIA (red)
  38. 38. Ultrasound cannot provide reliable imaging if there are poor acoustic windows (eg, bowel gas attenuation, diffuse vascular calcification, or metallic stents) or poor intrinsic echogenicity of the tissues. Duplex scanning is