Aneurysms, types of dissecting aneurysms, thromboangiitis obliterans (Buerger's disease), Raynaud phenomenon, venous diseases, hypertension, measurement of arterial blood pressure, arterial blood pressure regulation

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Department
Biomedical Science
Course
BMS 460
Professor
D.Rao Veeramachaneni
Semester
Fall

Description
4 November Aneurysms: localized abnormal dilation of a blood vessel. Can be congenital or acquired True aneurysms involve a thinned arterial wall False aneurysms or pseudo-aneurysms involve a breach in the arterial wall and the formation of an extravascular hematoma which may exhibit pulsations Dissecting aneurysms which involves redirection of blood flow into the wall of the artery itself Acquired: major causes are atherosclerosis (abdominal aorta especially and in smokers) and hypertension Congenital: Berry aneurysms Types of Dissecting Aneurysms Type A: involves the ascending aorta and/or aortic arch Type B: involves the descending aorta or the arch Complications of aortic dissection Rupture: pericardial tamponade, hemothorax Occlusion of aortic branch vessels: carotid arteries (storke), coronary artery (MI), splanchnic arteries (organ infarction), renal arteries (acute renal failure), peripheral arteries (limb ischemia) Distortion of aortic annulus: aortic valve regurgitation Thromboangiitis Obliterans (Buerger’s Disease) Vasculitis which leads to vascular insufficiency and is characterized by segmental thrombus formation and acute and chronic inflammation of medium and small arteries primarily of the tibial and radial arteries. Found mainly in heavy smokers before 35 years of age. Correlation with smoking is likely related to toxic effect on endothelial cells or an immune response to toxins in smoke. Impaired endothelial-development vasodilation common Raynaud Phenomenon Exaggerated vasoconstriction of digital arteries and arterioles usually due to cold temperatures Can also occur with arterial disease Vascular changes cause paroxysmal pallor or cyanosis of digits of feet and hands Usually benign but can result in atrophy of skin and subcutaneous tissue – even muscle Venous Diseases Varicose veins (superficial) – due to elevated venous pressure and lack of vessel wall support – common, familial tendency Problems: edema, pain, thrombosis but embolism rare Deep vein thrombosis (DVT) – life threatening and most common in veins of calves. Prolonged immobilization and heart failure (stasis) are important predisposing conditions but also polycythemia and systemic hypercoagulability as results from pro-coagulant factors from tumor cells and smoking. Vascular damage also may cause DVT. Pulmonary embolism is life-threatening (600,000/year) Others: esophageal varices due to portal hypertension and if ruptures occur → serious condition. Hemorrhoids: varicose dilations of anal-rectal junction – due to pelvic congestion from pregnancy or constipation. Spider veins: dilated small veins near skin Hypertension or the “silent disease” 60,000,000 in U.S. affected 1,000,000,000 people worldwide By 2025 – 1,500,000,000 people will be affected worldwide Leading cause of death worldwide One of world’s greatest public health issues By age 75 years, 90% of men and women in U.S. will have hypertension 140/90 mm Hg – hypertensive. But correlations to cardiovascular disease occur above 115/75 mm Hg Blood pressure variations along vascular tree and blood pressure terms Pulse pressure = systolic blood pressure – diastolic blood pressure Mean arterial pressure = 1/3 (pulse pressure) + diastolic blood pressure MABP = CO x TPR = SV x HR x TPR = (EDV – ESV) x HR x TPR Factors affecting arterial blood pressure Stroke volume/inotropy Distensibility of aorta/larger arteries Heart rate Systemic vascular resistance (vascular tone) Blood volume/venous constriction Hematocrit Measurement of Arterial Blood Pressure Korotkoff (1905) sounds using auscultatory method with cuff/stethoscope Phase 1: initial tapping = systolic blood pressure Phase 2: murmuring or swishing sounds Phase 3: increase in intensity and crispness of sounds Phase 4: muffling of sounds Phase 5: disappearance of sounds = diastolic blood pressure Older patients may exhibit an “auscultatory gap” where the Korotkoff sounds disappear and reappear 20 – 40 mm Hg later as cuff is deflated and may be caused by arterial pressure fluctuations. Result is underestimation of systolic blood pressure Cuff pressure above 110 mm Hg No blood flow No sound Cuff pressure between 70 and 110 mm Hg Turbulent flow in compressed artery makes audible vibrations (Korotkoff sounds) Cuff pressure below 70 mm Hg Laminar flow in noncompressed artery makes no sounds Systolic pressure – beginning of sounds Diastolic pressure – end of sounds Arterial Blood Pressure Regulation Arterial blood pressure is controlled by short-term and long-term mechanisms which affect the physical components of the factors determining arterial blood pressure. Neural, hormonal, endothelial and renal factors interplay to maintain stability in the face of changing internal and external demands. Short-term Regulation of Arterial Blood Pressure ABP = SV x HR x TPR Arterial baroreceptor reflex is rapid – seconds Responsiveness of arterial baroreceptors declines with age due to age related stiffness of vessel walls associated with baroreceptors and with hypertension and diabetes Within days of elevated arterial blood pressure, the baroreceptors reset to a higher level (fewer action potentials produced for given arterial blood pressure [stretch]) Long-term Regulation of Arterial Blood Pressure Increases in extracellular fluid volume (increased intake or decreased output) produces increases in CO and SVR (mediated by local vasoconstriction to protect against high- flow damage) → elevated BP Normally the kidney will return blood pressure to normal but in hypertension renal function may be altered Increased extracellular fluid volume → increased blood volume → increased mean circulatory filling pressure → increased venous return of blood to the heart → increased cardiac output Increased arterial pressure Autoregulation → increased total peripheral resistance → increased arterial pressure Venous return: equals cardiac output; volume of blood returned to heart by vena cava or pulmonary vein in one minute Mean circulatory filling pressure: pressure in vascular system (anywhere) when the heart is stopped. Provides measure of “overfilling of vascularity” and related to venous tone and blood volume Elevations in sodium which are eliminated by the kidney less rapidly than water contribute to elevated blood pressure Increased serum sodium level → increases osmolality → increases ADH secretion → increases blood pressure Renin-angiotensin-aldosterone system (RAAS) important regulator of BP but not the only one implicated in hypertension (baroreceptors, va
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