elevated systolic BP accompanied by normal diastolic BP (<90)

wide pulse pressure; differences due to reduced vascular compliance of larger arteries espec. the aorta; mostly in people older than 65; asymptomatic usually

fat and fibrin deposits in the intrarterial area; ischemic conditions from head to toe

form of arteriosclerosis in which thickening and hardening of the vessel are caused by the accumulation of lipid-laden macrophages within the arterial wall, which leads to formation of plaque not single disease but process that can affect vascular systems throughout body - ischemic syndromes leading contributor to CAD and cerebrovascular disease Clinical Manifestations: inadequate perfusion of tissues by vessel obstruction stroke and myocardial ischemia may occur

inflammatory disease; lesions progress from endothelial injury & dysfunction to fatty streak to fibrotic plaque to complicated lesion Progression Fig30-11 p1158 injury caused by risk factors question #7 and CAD risk factor Process injury - inflammation - cant make cytokines inflam. cytokines, toxic oxygen radicals, and heat shock proteins released macrophages adhere to injury macrophages release enzymes and radicals that cause further damage growth factors released that stimulate smooth muscle cell proliferation inflammation with oxidative stress (from LDL) and activation of macrophages is the primary mechanism (p1157,1158) fatty streak forms then plaque - can lead to rupture causing complicated plaque;

eventually occluding vessels like those in cardiac MI or brain Stroke

fissure or small tear in plaque - occlusion - constriction CM: Box30-1 p1171

Stable Angina: recurrent predictable chest pain lasting 3-5min, relieved my rest or nitro; caused my ischemia that is progressive

Prinzmetal angina: at rest (most likely to have infarction and die); unpredictable, caused by vasospasms at rest, occurs often during REM sleep

Unstable: result of reversible myo ischemia, plaque within coronary artery becomes complicated and unstable causing MI to follow soon

new-onset angina:angina that is increasing in freq. or severity; dyspnea, diaphoresis, anxiety

cell injury - cell death after 20min - many structural and functional changes p1172

- the myocardial damage repair **Table 30-7**

CM: sudden severe chest pain; heavy crushing pain; radiation to neck, jaw, back, shoulder, left arm; sweaty, clammy, cool; nausea n vomitting may occur

During MI, areas of ischemia may go out farther than the zone of infarction, they will heal over time but the area of necrosis will be scarred

Pressure of ventricle can sometimes blow out that area of necrosis causing immediate death

carditis: murmur heard, chest pain, audible friction rub, extra heart sounds, heart block, afib, prolonged PR interval complication: endocardial inflammation caused yrs later - valve stenosis and regurge - recurrent infective endocarditis

CM: fever, inflammation of joints, skin, nervous system, and heart  (carditis, corea erythema, polyneuritis)

  eventually may need surgical intervention to fix mitral valve

scarring and deformity of cardiac structures resulting from rheumatic fever (diffuse inflammation caused by a delayed immune response to infection with group A betahemolytic streptococci) crowding and poor hygiene are risk factors for acute rheumatic fever

-death and disability occur mainly in underprivileged population

-antibiotic given within first 9 days usually prevents rheumatic fever

-genetic predisposition noted

RF develops only as a sequel to pharyngeal infection -abnormal humoral and cell-mediated immune response to the M proteins on the bacteria that cross react with normal tissue

-diffuse, proliferative, and exudative inflammatory lesions develop in the connective tissues, especially in the heart, joints, and skin

-inflammation may subside before treatment leaving damage to heart valves and increased susceptibility to recurrent RF -10% develop RHD: begins as carditis, or inflammation of the heart

-primary lesion usually involves the endocardium, which lines the heart chambers and includes valves (swelling and erosion of leaflets)

-small clumps of vegetation form on eroded valve and chordae tendineae - lose elasticity and leaflets adhere to one another - scarring and shortening over time -inflammation penetrates myocardium

- localized fibrin deposits (aschoff bodies) develop that are surround by areas of necrosis -pericardial inflammation may occur from serofribinous effusion -Cardiomegaly and LSHF may occur with recurrent RF -conduction defects and afib occur

- True aneurysms: involve all three layers of the arterial wall and are weakening - either Fusiform or Circumferential

- False aneurysm: extravascular hematoma that communicates with the intravascular space (common cause is leak between vascular graft and natural artery) - Saccullar aneurysm: spherical - Ventricular wall aneurysm occurs when intraventricular tension stretches the noncontracting infarcted muscle - infarct expansion - weak thin layer of necrotic muscle - fibrous tissue that bulges with each systole (“reservoir” for some stroke volume)

CO depends on SV(contractility, preload, afterload) and HR - Contractility reduce when disease affects myocyte activity (MI most common cause) - Ventricular remodeling then occurs - hypertrophy and dilation of the myocardium - causing progressive myocyte contractile dysfunction (Fig30-38 p1191) - decreased contractility = SV fails = LVEDV increases = dilation of heart and increased preload - increased afterload results from increased peripheral vascular resistance seen in HTN (details 1190 last paragraph) - Great Fig30-41 p1192 for details of the cycle of LSHF

receives blood from lungs into l atrium into l ventricle then pushed to periphery, if weakened or  meet resistance because of HTN in periphery then backflow goes to l ventricle then l atrium then Lungs causing pulmonary edema

LEFT think LUNG symptoms

the inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at a normal central venous pressure

- results from LSHF

- pressure from back flow in the pulmonary circulation rises causing increased resistance to right ventricular emptying (dilate and fails)

-pressure in systemic venous circulation rises resulting in jugular vein distention, peripheral edema, and hepatosplenomegaly

- other causes include: COPD, cystic fibrosis, ARDS, right ventricular MI, cardiomyopathies, pulmonic valvular disease

r atrium via vena cava into right ventricle into right lung…if lung is diseased and bloood flow is restricted OR had a right sided MI then there is back flow to right ventricle and that increased volume will back flow into atrium and vena cava and cause congestion in liver, edema in legs, jugular distention

aka Thromboangiitis obliterans

-occurs in young men who smokes cigs a lot

- an inflammatory disease of the peripheral arteries

- 95% assoc. with smoking

- other 5% r/t frostbite, trauma, or use of sympathomimetic drugs

- inflammatory lesions accompanied by thrombi and sometimes vasospasms of arterial segments

- all of these eventually occlude & obliterate portions of small and medium sized arteries of the digital, plantar, tibial of feet & digital, palmar, ulnar of hands

- Patho: significant T cell activation and autoimmunity

- Chief Sx: pain and tenderness of affected area

- CM caused by sluggish blood flow: rubbor (redness from dilated capillaries and cyanosis (blood remaining in capillaries after oxygen leaves it); chronic ischemia causes skin to thin and become shiny; thick nails and malformed; can lead to gangrene; assoc. with cerebrovascular disease and rheumatic sx

- cessation of smoking is main Tx

- secondary to systemic diseases particularly collagen vascular disease (scleroderma), rheumatoid arthritis, chemo, cocaine use, hypothyroidism, pulmonary HTN, thoracic outlet syndrome, serum sickness, vasculitis, malignancy (r/t to malig can be severe and diagnostic of previously undx cancer), or long-term exposure to cold or vibrating machinery attacks of vasospasm in small arteries and arterioles of fingers and less commonly, toes

Sx of phenomenon and disease are same..causes different

- primary vasospastic disorder of unknown origin

- affects young women and consist of vasospastic attacks triggered by brief exposure to cold or by emotional stress

- BVs demonstrate endothelial dysfunction w/ decreases nitric oxide production and increased endothelin-1 activity; imbalances in endothelium-derived vasodilators and vasoconstrictors

CM: changes in color and sensation in digits

any of a group of disease caused by obstruction of large peripheral arteries secondary to atherosclerosis, inflammatory processes, embolism, or thrombus formation that causes ischemia

- 12million in US have PAD

- prevalent in ppl with diabetes; risk are same as those for atherosclerosis (smoking, HTN, diabetes, increased LDL, decreased HDL, autoimmunity)

- lower extremity ischemia, resulting from arterial obstruction

- gradual or acute - gradual may cause intermittent claudication

- if thrombus occurs over atherosclerosis, perfusion ceseases and severe pain, loss of pulses, and skin color change occur in affected extremity

- Often asymptomatic; Dx: look for bruits and perform noninvasive doppler measurement of blood flow

Occurs in lower extremities

Especially in diabetes

Referred to PAD or PVD

Complain of pain with exercise, intermittent claudication; cool hairless lower leg with diminished pulses (pedal diminish first)

arises form VENOUS insufficiency, p1143; circulation to the extremities can become so sluggish that the metabolic demands of the cells for oxygen nutrients, and waste removal are barely met, therefore any trauma or pressure can lower the oxygen supply and cause cell death and necrosis aka ulcer

Ulcer due to fibrosclerotic remodeling of skin

the anterior and posterior cusps of the mitral valve billow upward (prolapse) into the atrium during systole

- most common cause is myxomatous degeneration of the leaflets in which the cusps are redundant, thickened, and scalloped because of changes in tissue proteoglycans, increased proteinases, and infiltration of myofibroblasts

- chordae tendineae may be elongated cause valve cusps to stretch forward

- mitral regurgitation occurs if the ballooning valve permits blood to leak into the atrium

**most common valve disorder in US

- 1-3% of adults; more in young women;

autosomal dominant and x-linked inheritance; associated with inherited connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta); genetic and environmental disruption of valve development during 5-6th wk gestation

p1183

Many are completely asymptomatic

- regurgitant murmur or midsystolic click may be heard

- palpitations r/t dysrhythmias, tachy, lightheadedness, syncope, fatigue (espec. in the morning), lethargy, weakness, dyspnea, chest tightness, hyperventilation, anxiety, depression, panic attacks, atypical chest pain

- most common complication is infective endocarditis

All stages associated with TARGET ORGAN DISEASE: the vascular system feeds specific organs : heart kidney eye and brain

MI, stroke, kidney disease, or eye disease

p1149 fig30-2

The systolic pressure is MOST significant factor in target organ damage

low BP caused by altered body chemistry, drugs, prolonged immobility, starvation, exhaustion, volume depletion, venous cooling (vasodialtion from progesterone in pregnancy espec prima gravidum)

  CM: dizziness, blurry, loss of vision, syncope

most likely aortic before expands so big, p1158, between the intima and media that aneurysm may begin and expand causing a stripping of the intima and media that is very painful; before splitting starts pt may have difficulty eating or swallowing