chapter 26 & 28: disorders of blood flow, blood pressure regulation, and cardiac rhythm

Arteries

carry blood away from the heart; have thick, elastic, muscular walls

veins

carry blood to the heart; have thinner walls than arteries

capillaries

smallest blood vessels responsible for exchange between blood and interstitial fluid

tunica interna

endothelium (inner layer)

tunica media

smooth muscle (middle layer)

tunica externa

adventitia (outer layer)

functions of vascular endothelium

regulates thrombosis, controls the transfer of substances, regulates blood flow

regulates thrombosis

releases tissue plasminogen activator, which helps dissolve blood clots

controls transfer of substance

movement of molecules between blood and surrounding tissues

regulates blood flow

releases nitric oxide, which relaxes vascular smooth muscle and causes vasodilation

function of vascular smooth muscle

regulates blood pressure and systemic vascular resistance; SNS activates the release of norepinephrine, which binds to alpha-1 receptors on vascular smooth muscle (cause vasoconstriction, increased VR and BP)

blood pressure

force exerted by circulating blood against the walls of blood vessels, especially the arteries

systolic pressure

exerted when blood is ejected from ventricles during contraction (120 mmHg)

diastolic pressure

sustained pressure when ventricles relax (80 mmHg)

pulse pressure

difference between systolic and diastolic BP

factors affecting BP

cardiac output, blood volume, and blood vessel diameter

cardiac output

volume of blood pumped by one ventricle per minute

blood volume

Total amount of blood circulating in the body.

increased blood volume

increases cardiac output and BP

decreased blood volume

decreases cardiac output and BP

blood vessel diameter (peripheral resistance)

vasoconstriction increases resistance and BP; vasodilation decreases resistance and BP

short term blood pressure regulation

managed by SNS; regulates blood pressure rapidly by adjusting heart activity and blood vessel diameter

baroreceptor reflex

primary neural mechanism for short-term blood pressure regulation; works through negative feedback loop involving pressure sensors and the autonomic nervous system

baroreceptors

stretch-sensitive receptors located in the walls of the carotid sinuses and aortic arch; detect changes in BP and signal the brain to adjust heart rate, cardiac output, and blood vessel diameter

hormonal regulation

slower, long-term process that maintains blood pressure by adjusting blood volume and systemic vascular resistance

Antidiuretic Hormone (ADH)

increases water reabsorption by the kidneys, raising blood volume and BP

renin-angiotensin-aldosterone system

major mechanism of long-term BP regulation; activated when BP, blood volume, or kidney perfusion decreases; raises BP through vasoconstriction and increased sodium and water retention

epinephrine

increases HR and cardiac contractility and can cause vasoconstriction

steps of RAAS

1.) low BP causes kidneys to release renin

2.) renin: converts angiotensinogen into angiotensin I

3.) ACE: converts angiotensin I into angiotensin II

4.) Angiotensin II: causes vasoconstriction and stimulates aldosterone release

5.) Aldosterone: increases sodium and water retention by the kidneys

6.) result: blood volume and BP increase

lipoproteins

particles made of lipids and proteins that transport cholesterol and triglycerides through the bloodstream

chylomicrons

transport dietary triglycerides

VLDL (very low density lipoprotein)

transport triglycerides synthesized in liver

LDL (low density lipoprotein)

main carrier of cholesterol

HDL

high-density lipoprotein; 50% protein

low-density lipoprotein

bad cholesterol; transports cholesterol from the liver to body cells; high LDL levels contribute to atheroma formation

high-density lipoprotein

good cholesterol; transports excess cholesterol from peripheral tissues back to the liver; cholesterol is broken down or converted into bile acids and can be eliminated through bile and feces; helps remove excess cholesterol form tissues and supports cardiovascular health

hypercholesterolemia

high level of cholesterol in the blood; total serum cholesterol of 240 mg/dL or higher; can contribute to heart attack, stroke, or other cardiovascular event associated with atherosclerosis

primary hypercholesterolemia

mainly caused by genetic factors; develops independently of other medical conditions; ex: familial hypercholesterolemia

secondary hypercholesterolemia

result of other medical conditions, medications, or lifestyle factors; ex: diabetes mellitus, obesity, and hypothyroidism

arteriosclerosis

general term for the thickening, hardening, and loss of elasticity of the arteries; arteries become stiff, making it harder to maintain normal blood flow

atherosclerosis

type of arteriosclerosis characterized by buildup of fatty plaques called atheroma in the walls of large and medium-sized arteries; plaques gradually narrow the arterial lumen and may restrict or block blood flow

atheromas contain

cholesterol and other lipids, inflammatory cells, and fibrous tissue; calcium may accumulate over time

stable plaques

have thick fibrous cap; usually grow slowly and narrow the artery over time; may cause reduced blood flow; less likely to form blood clots or emboli

step 1 of atherosclerosis formation

endothelial injury: damage to endothelium triggers inflammatory response

step 2 of atherosclerosis formation

LDL enters and accumulates in damaged arterial wall

step 3 of atherosclerosis formation

LDL becomes oxidized, promoting inflammation and free radical formation

step 4 of atherosclerosis formation

endothelial cells release inflammatory chemicals that attract immune cells to affected area

step 5 of atherosclerosis formation

macrophages engulf oxidized LDL cholesterol and become foam cells

Step 6 of atherosclerosis formation

smooth muscle cells migrate and multiply within the arterial wall: form a fibrous cap over fatty core

unstable plaque

have thin fibrous cap; more likely to rupture or erode; can trigger rapid blood clot formation; may completely block the artery or become an embolus

nonmodifiable factors of atherosclerosis

Risk factors that cannot be changed; age (risk increases as you age); genetic or familial factors (family history and inherited conditions can increase risk)

modifiable factors of atherosclerosis

risk factors that can be reduced or managed; obesity and sedentary life-style, cigarette smoking, diabetes mellitus, poorly controlled hypertension

progression of atherosclerosis

fatty streaks, fibrous atheromatous plaque, complicated lesion

fatty streaks

earliest visible lesion of atherosclerosis; appear as thin, flat, yellow discolorations in the intima that progressively enlarge

fibrous atheromatous plaque

develops as lipids accumulate and fibrous cap forms over lipid core; gradually thickens and narrows the arterial lumen

complicated lesion

advanced, more complex atherosclerotic plaque; may rupture, cause ulceration, hemorrhage, and blood clot

peripheral arterial disease

narrowing or blockage of arteries supplying the lower extremities due to atherosclerotic plaque buildup; common cardiovascular condition

symptoms of PAD

may cause no noticeable symptoms until blood flow becomes significantly reduced; symptoms appear when an artery is narrowed by more than 50%, depending on the artery involved and the patient's level of physical activity; may manifest acutely when thrombi or emboli compromise blood flow

classic symptoms of PAD

intermittent claudication; leg pain or cramping during walking or exercise that improves with rest, gastrocnemius muscle requires increased oxygen during exercise, narrowed arteries limit blood flow and oxygen delivery, causing ischemic pain

advanced symptoms of PAD

severe arterial narrowing or occlusion can cause reduced blood flow even at rest; pain in legs or feet at rest, weak distal pulse; redness in depended position due to gravity; thinning of skin, non-healing sores, nail changes

treatment of PAD

walking slowly, avoid injury, antiplatelet agents, bypass grafting, angioplasty

acute arterial occlusion

sudden blockage of arterial blood flow caused by a thrombus or embolus, often occurring in patients with pre-existing PAD

arteries most involved in atherosclerosis

arteries that supply the heart, brain, kidneys, lower extremities, and small intestine

larger artery complications of atherosclerosis

thrombus formation and weakening of the vessel wall; can lead to aneurysm

medium-sized artery complications of atherosclerosis

ischemia and infarction due to vessel occlusion are more common

five "P's" of acute arterial occlusion

pistol shot (acute) pain; pulselessness, paralysis (muscle weakness), paresthesia (burning, numbness), pallor, polar (cold skin)

thromboangitis obliterans

rare, progressive, non-atherosclerotic inflammatory disease that affects small- and medium-sized blood vessels characterized by inflammation, narrowing and occlusion, and reduced blood flow

inflammation in TAO

blood vessels become inflamed and swollen

narrowing and occlusion in TAO

inflammation causes the vessels to narrow or become blocked by blood clots (thrombosis)

reduced blood flow

blockage severely reduces blood flow to fingers, toes, hands, and feet

manifestations of TAO

more commonly affects men older than 45 years; early symptoms: pain at rest; affects plantar and digital vessels in foot; cause ischemic ulcerations, gangrene

aneurysm

localized dilation and weakening of an arterial wall, often associated with damage to the middle layer

saccular aneurysm

localized, sac-like bulge on one side of the arterial wall

fusiform aneurysm

circumferential dilation along a section of artery

dissecting aneurysm

occurs when a tear develops in the inner arterial layer, allowing blood to enter and separate the layers of the arterial wall; hemorrhage into vessel wall forms a blood-filled channel

berry aneurysm

commonly occurs in the circle of Willis in the brain; consists of a small, spherical vessel dilation

fusiform and saccular aneurysm

commonly occur in the thoracic or abdominal aorta; characterized by gradual and progressive enlargement of the aorta

abdominal aortic aneurysm

wall of aorta weakens and stretches; frequently asymptomatic (risk of clot formation, rupture, hemorrhage; blowing sound (bruit) heard over the affected artery due to turbulent blood flow; pulsating abdominal mass felt during palpation

dissecting aneurysm manifestations

more common in men aged 40-60 with a history of hypertension; abrupt excruciating pain (ripping or tear of chest or back pain), BP and pulse unobtainable, high mortality risk due to severe internal bleeding

varicose veins

enlarged, dilated, and tortuous superficial veins, commonly found in the legs; develop due to weekend vein walls or damaged valves

development of varicose veins

faulty valves allow blood to flow backward and accumulate in the veins; increased venous pressure causes the veins to enlarge and become twisted; appear as irregular, purplish, bulging structures in the legs

risk factors of varicose veins

familial tendency, increased BMiI, parity

thrombophlebitis

inflammation of a vein associated with formation of a blood clot

signs and symptoms of thrombophlebitis

may be asymptomatic or go unnoticed; aching or burning sensation; tenderness, redness, and swelling around affected vein

pulmonary embolism

risk caused by thrombophlebitis; obstruction of pulmonary arteries by emboli

virchow's triad

three major factors that increase the risk of venous thrombosis; venous stasis: sluggish or reduced blood flow, endothelial injury, increased blood coagulability

hypertension

high blood pressure (reading falls at or above 130/80 mmHg); common, may occur in any age group; frequently asymptomatic in early stages

symptoms of hypertension

vague, nonspecific; fatigue, morning occipital headache

primary (essential) hypertension

most common type of HTN; develops gradually over many years with no identifiable cause; pathophysiologic mechanism is increased SNS activity

arteriolar vasoconstriction

increases total peripheral resistance (TPR)

increased heart rate and cardiac contractility

increases cardiac output

stimulation of RAAS

promotes sodium and water retention, increasing blood volume

secondary hypertension

high BP caused by an identifiable underlying condition; commonly caused by renal disease, endocrine disorders, and pheochromocytoma

Renal disease

kidney disorders that affect fluid balance and BP regulation

endocrine disorders

hormonal imbalances that increase blood pressure

Pheochromocytoma

rare tumor of the adrenal medulla that releases excess catecholamines, such as adrenaline and noradrenaline

malignant hypertension

severe, rapidly progressive form of hypertension that can cause acute damage to vital organs; extremely elevated blood pressure, often with diastolic pressure around or above 120 mmHg; can cause serious complications involving the brain, heart, kidneys, and eyes

left ventricular hypertrophy

left ventricular wall thickens because the heart must work harder to pump blood against increased vascular resistance (increased after load); thickened heart muscle may become stiff and less efficient, potentially leading to heart failure

nephrosclerosis

damage and hardening of small renal blood vessels due to long-standing hypertension

glomerular damage

reduced blood supply and injury to the glomeruli