patho 2 there are already way too many

Risks for vascular insufficiency arterial

smoking, atherosclerosis, inflammatory (buergers), trauma, emboli from Left Ventricle, vasospasm, diabetes mellitus

Atherosclerosis

buildup in vessels

Risk for vascular insufficiency venous

stasis of blood flow (immobility, R heart failure, prolonged standing, obesity, pregnancy), trauma, hypercoagulable (high platelets, high hematocrit)

Left side of heart

arterial (aorta) sends oxygenated blood to rest of body

Venous blood

less pressure than arterial blood

Obstruction

thrombosis, embolus, vasospasm, inflammation, arteriosclerosis, acute arterial occlusion

Mechanical alterations

arteriovenous fistulas, aneurysms, acute arterial occlusion

Thrombosis

blood clot in vessel or chamber of the heart

Ischemia

Arterial thrombosis

Edema

venous thrombosis (swelling below the clot)

General thrombosis risk factors

hypercoagulation conditions, pump failure, dysrhythmias, aging, trauma, drugs

Arterial risk factors

arteriosclerosis/atherosclerosis

Venous risk factors

immobilization

Venous

LUNGS

Thrombosis arterial CM

intermittent claudication, cool, cyanotic, painful ulcer around one toe

Thrombosis venous CM

none or life threatening PE, calf/groin tenderness, swelling, Homan’s sign

Thrombosis treatment

anticoagulation, thrombolytic drugs,antiembolic stockings, sequential compression devices, ambulation ASAP, surgery

Embolus

clot in the bloodstream (may travel to distant point)

Ischemic stroke

embolism leaving L ventricle

Pulmonary embolism

embolism leaving R ventricle

Embolus treatment

embolectomy or filter

Emboli produced by other causes

fat, malignant neoplasm or tumors, collection of bacterial/infectious exudate, air, amniotic fluid

Vasospasm

sudden, involuntary constriction of arterial smooth muscle \= obstruction of flow,

Vasospasm cause

hormonal changes, food additives, or environmental factors

Vasospasm manifestations

angina, hemorrhagic stroke, migraine HA

Raynaud syndrome

extreme vasoconstriction arterial response in hand and fingers to cold and stress; primarily young women (genetic tendency)

Raynaud syndrome causes

digital arteries go into spasm, defined as episodes of blue and white color changes in digits induced by cold or emotional stimuli followed by red discoloration during hyperemia recovery phase

Raynaud syndrome CM

throbbing, burning pain, erythema (red, white, blue disease)

Inflammation

can increase risk of thrombotic process

Vasculitis

inflammation of the inside of an artery

Arteritis

inflammatory process of autoimmune origin in arteries

Phlebitis

Inflammation in a vein

Thrombophlebitis

inflammation with clot in a vein

Thromboangitis oliterans (buerger disease)

rare inflammatory condition, tobacco use, men under 40, jewish/asian descent, remission and exacerbation, genetic, over immune response

Buerger disease CM

pain, intermittent claudication, decreased pulse, cyanosis

arteriosclerosis

hardening of the arteries, thickening and narrowing of lumen in small arteries

Atherosclerosis

lipids collect along lumen and produce narrowing and reduction blood flow/inflammatory response

Atherosclerosis

underlying pathology of HTN, cardiac & renal disease, PVD & CVA; effects humans with cholesterol rich diet, begins in childhood developing slowly until widespread in old age (recommended at 5 years old); may be accelerated by genetic & environmental factors

Atherosclerosis CM

angina, MI, HTN, thrombotic strokes, intermittent claudication, gangrene

Atherosclerosis treatment

non pharmacologic such as weight reduction, stopping smoking, exercise, low fat diet, then if not successful drug therapy added, or surgery (laser angioplasty, stents, CABG)

Mechanical compression

obstruction of blood flow due to trauma, constriction, swelling; may lead to hypoxia, ischemia, or tissue necrosis; external forces to the vascular system may result in partial or complete obstruction

Mechanical compression caused by

trauma, tight casts/dressing/stocking, compartment syndrome

Aneurysms

weakness

Aneurysms

early detection \= definitive repair, permanent localized dilation of arterial wall weakens and bulges outward, often found in cerebral circulation. Thoracic and abdominal aorta; dissecting aortic

Aneurysms are

medical emergencies and treated medically or surgically

Aneurysms degenerative etiology

years to decades to enlarge

Aneurysms infectious or traumatic etiology

days to months

Aneurysms etiology

atherosclerotic changes in vessel, trauma, congenital weakness, infection, or inflammation

Aorta

Vessel with most pressure

True Aneurysms

all 3 layers of vessel involved

Saccular

weakening confined to one side of vessel

Fusiform

weakening of both sides of vessel wall

False Aneurysms

at least one layer of vessel is unaffected

Dissecting

tear in the vessel wall that creates a channel of blood flow between the layers of the vessel (much more dangerous, seperated and even weaker)

Dissecting

much more dangerous, pops easier

Stent

allow blood flow

Arteriovenous fistulas

abnormal communication between arteries & veins, usually congenital in origin, symptoms depend on size and location, may result in alterations in 02 to involved tissues

Acute arterial occlusion

absence of arterial circulation, embolism lodges in major artery followed by decreased circulation, due to thrombus / embolus / trauma / vasospasm, usually surgical emergency

*Acute arterial occlusion CM

6 “Ps” pallor (white), paraesthesia (numbness), paralysis (can't use), pain, polar (cold), pulselessness

Acute arterial occlusion treatment

figure out what is causing the loss of circulation and fix it

Alterations in venous flow

caused by obstruction to flow or structural alterations, incompetent valves \= varicose veins / chronic venous insufficiency / obstruction by DVT, overstretching of the valves \= excess venous pressures resulting in backflow of blood

Alterations in venous flow CM

edema, venous stasis, ulcers, pain

Varicose veins

superficial , will not die from these

Varicose veins

incompetent valves (reduced venous return, increased venous pressure and venous stasis), causes edema and superficial vein that is twisted / enlarged / darkened / raised / tortuous, primary varicosities may be familial

Varicose veins secondary causes

extrinsic venous compression, prior DVT, congenital causes and arteriovenous fistulas

Varicose veins CM

distended veins, heaviness in legs, swelling in lower extremities, stasis ulcers

Varicose veins treatment

sclerotherapy, removal

Chronic venous insufficiency

advanced valvular incompetence or blockage within venous system involving deep veins, skin pigmentation becomes brown, venous stasis ulcers develop, aching and cramping in legs

Deep vein thrombophlebitis

extremity edema, general leg pain, fever, redness, tenderness, positive homans sign , high risk of PE

Deep vein thrombophlebitis

chronic venous insufficiency, may be life threatening, injury to lining of vein causes decreased circulation and stimulates aggregation of platelets which occluded vessel, emboli may break away and travel to pulmonary circulation

Superficial thrombophlebitis

local inflammation (warm, tender, red, swollen), collateral veins minimize edema, low risk of PE

Lymphatics

transport 25 to 50% all circulating blood proteins per day, located primarily in subcutaneous tissue

Lymphatic structure

thin walled and resemble veins, range in size from capillaries to large vessels, intermittent valves that extend into lumen, walls have contractile fibers to propel lymph along vessel, changes in capillary or interstitial pressure increases filtration into tissue resulting in edema, lymphedema results from impairment in circulation of lymph

Lymphedema

abnormal buildup of lymph fluid in dermal and subQ tissues due to impairment in circulation of lymph, changes in capillary pressures increase filtration and overwhelm the lymphatic circulatory system

Secondary lymphedema

lymphatic vessel damage due to trauma, recurrent infections, obstructive mass, infiltrative processes and radiation (breast cancer)

Secondary lymphedema CM

regional edema and thickened subcutaneous tissue

Arterial blood pressure

produced by force of L ventricular contraction overcoming resistance of aorta to open aortic valve; arterial diameter affects resistance therefore BP

Determinants of systemic blood pressure

1. CO and the resistance to ejection of blood from the heart (afterload) 2. End diastolic volume is the preload, 3. Systemic vascular resistance (afterload) determined by the radius of arterioles and degree of vessel compliance

*Afterload

systemic vascular resistance (what blood has to push against)

Systolic BP

peak pressure

Diastolic BP

lowest pressure

Stroke volume

primary factor influencing systolic pressure

Systemic vascular resistance

major determinant of diastolic pressure

Mean arterial pressure

calculated average pressure within circulatory system throughout the cardiac cycle

Short term regulation of BP

baroreceptors monitor change and activate SNS, parasympathetic nervous system slows HR

Long term regulation of systemic BP

regulated by neural, hormonal, renal systems (increased ECF volume \= increase CO and SVR; increase serum Na \= increased ADH secretion), RAAS (kidneys check oxygen in blood)

Direct measurements of BP

requires intra arterial catheter to transduce arterial fluid pulsations into electronic signals, catheter placed in radial artery, most accurate

Indirect measurement of BP

brachial artery using stethoscope or automated system, careful technique to ensure accuracy

Pulse pressure

systolic minus diastolic pressure

Hypertension (HTN)

sustained BP greater than normal, need 2 BP greater than normal to diagnose, not single disease but syndrome with multiple causes

Primary HTN

essential HTN (cause is unknown)

Secondary HTN

cause is known (secondary to other causes)

Hypertension

most common diagnosis in US, increased morbidity and mortality associated with heart disease, renal disease, peripheral vascular disease & stroke

Hypertension predictor of

CVA, CAD, CHF, renal disease

Primary HTN

idiopathic, most common form, rare prior to age 10, major risk factor for CV disease

Primary HTN pathogenesis

vasoconstriction or narrowed peripheral blood vessels, causes increased peripheral resistance, increased workload & more pressure (afterload); damage to renal blood vessels increase fluid & waste, kidney failure results

Primary HTN treatment

lifestyle modifications 1st (wt loss, exercise, ETOH moderation, decrease Na intake), drug tx for HTN affects HR, systemic vascular resistance or SV

Primary HTN outcomes

Brain, eyes, kidney, heart “silent killer” (damage has already occurred to organs), end organ damage (renal failure, stroke, heart disease, damage to arterial system, speeds up *atherosclerosis \= CV disease, increased myocardial work \= heart failure, microcirculation of eyes (can go blind), increased pressure in cerebral vasculature \= hemorrhage)

Secondary HTN causes

renal artery stenosis, pregnancy induced, pheochromocytoma, sleep apnea, hyperaldosteronism, obesity, renal disease, contraceptive use, cushing syndrome, drug induced, hyperthyroid, coarctation of aorta, polycythemia

HTN clinical manifestations

may be asymptomatic, HA, dizziness, nausea vomiting, visual disturbances, renal insufficiency