Part 3: Blood Flow and Pressure

what is acute arterial occlusion

sudden interruption of blood flow in the artery

define thrombus

erosion or rupture of a plaque; fancy word for blood clot

define thromboembolus

a blood clot that can travel (often from the heart, but can detect from anywhere) that get stuck where an plaque has already created an occlusion

why is arterial blood flow so important

because it gives our tissues oxygenated blood

unstable is to acute, as stable is to

chronic

the seven P’s of an acute arterial occlusion

1. pistol shot; meaning everything happens fast (ACUTE)

2. pallor; white color

3. polar; cold to tough

4. pulseless

5. pain

6. paresthesia; numbness and tingling

7. paralysis; won’t be able to use leg anymore

diagnosis of acute arterial osculation

using an doppler to find a pulse or arteriogram

treatment of acute arterial occlusion

Thrombolytic therapy

Embolectomy

Anticoagulation

so either removing clot or give medication to break up clot and thin blood

acute arterial occlusion vs peripheral artery disease

• Acute arterial occlusion is characterized by a sudden, complete blockage of an artery, leading to immediate and severe symptoms.

• Peripheral Artery Disease involves a gradual narrowing of arteries over time, resulting in chronic symptoms and an increased risk of cardiovascular events.

  Acute arterial occlusion demands urgent attention, while PAD is a chronic condition that may be managed with lifestyle changes and medical interventions.

peripheral arterial disease (PAD) is to

atherosclerosis in the extremities

peripheral arterial disease (PAD) is most common

arteries of LEG

-femoral & popliteal

risk factors for peripheral arterial disease (PAD)

Age

Race (African America 2x risk)

Smoking

Diabetes

Hyperlipidemia “high cholesterol”

Hypertension

in peripheral arterial disease (PAD) oxygen to the tissue is

LOW

what is the PATHO behind peripheral arterial disease (PAD)

decreased flow and tissue oxygenation

how do the signs of symptoms occur

GRADUAL; thus meaning overtime

signs and symptoms of peripheral artery disease

1. Claudication; pain in legs with walking/ oxygen demands is higher when moving but have blockages

2. Thin skin

3. Brittle nails

4. Muscle atrophy; shrink in size

5. Cool feet

6. Dependent rubor; when legs raised up the local blood vessel are using auto-regulation to dilate and bring more blood flow to the area making foot RED IN NATURE

7. Delayed wound healing; if there is poor blood flow then it will be harder to fight off infections

complications of peripheral arterial disease (PAD)

Ulcer

Necrosis; lack of oxygen = death of tissues

Poor wound healing

Amputation

how is peripheral arterial disease (PAD) diagnosed

by doing an Ankle-brachial indices (ABI)

Ankle-brachial indices (ABI)

done by comparing BP in leg to BP in arm

<0.9 ration = PAD

which indicates poor circulation within the leg

what is the treatment for peripheral arterial disease (PAD)

*WALKING TO INCREASE COLLATERAL CIRCULATION

-refers to the network of smaller blood vessels that can develop and provide an alternative route for blood flow when the main arteries are partially blocked

by forcing the body to create blood vessels around

other treatment options for peripheral arterial disease (PAD)

Risk factor modification; for instance reducing blood pressure / control blood sugar / loose weight / control cholesterol levels

Foot protection

Pharmacological

Catheter interventions

Fem pop bypass

would you put compression socking on a person with peripheral arterial disease (PAD) , what is the reasoning behind it?

PAD involves the narrowing of arteries, restricting blood flow to the extremities, and compression stockings are designed to provide pressure, which could further compromise blood circulation

NO, because we would be restricting blood flow even more than it already is

-really only recommended/ useful in venous disease; with damaged valves and muscles

what is Raynaud’s Disease/ Phenomenon

intense VASOSPASM of arteries/ arterioles in fingers and less often toes

-not a cause of plaques instead from vasospasm in the arteries

what is the primary cause of Raynaud’s Disease/ Phenomenon (also happens to be the most common as well)

unknown

-common in young women

-exposure to cold and emotional stress, possibly hyperactive SNS response

what is the secondary cause of Raynaud’s Disease/ Phenomenon

associated with diseases/ situations that cause VASOSPASM

collagen diseases / frostbite / trauma (FTC)

signs and symptoms of Raynaud’s Disease/ Phenomenon

skin pale to cyanotic, cold sensations, numbness/ tingling

LATER PEROID OF hyperemia → redness, throbbing

why does this later period of hyperemia → redness, throbbing occur

due to autoregulation and vasodilation

treatment for Raynaud’s Disease/ Phenomenon

Eliminate triggers

Protect from trauma

Smoking cessation → as we know smoking causes damage to our blood vessels

what is an aneurysm

ballooning out of vessel wall (or chamber of heart)

-weakened or ballooning of a blood vessel or te chamber of the heart

why do aneurysms occur in arteries, not veins

because veins are good at dilating and holding lots of blood

-and there is a lot of pressure in the arteries → lots of pressure over time can start to weaken the vessel wall

define true aneurysms

bound by complete vessel wall; when all three layers are weakened

-falciform or saccular

the entire vessel wall weakens, causing a bulge or dilation in the artery or vessel thats really all

falciform vs saccular

fusiform happens on both side whereas saccular only occurs on one side = unilateral

false (pseudoaneurysm) aneurysm

tear in arterial wall with extravascular hematoma

-tear in the wall so clot starts to develop on outside of artery

dissecting aneurysm

Intimal tear

Blood between layers of vessel wall

-tear in the intimal layer and blood is developing between the layers

why is a dissecting aneurysm considered to be “life threatening”

A dissecting aneurysm is life-threatening because it involves a tear in the artery wall, putting it at risk of rupture. If the weakened artery ruptures, it can lead to severe internal bleeding, disrupting blood flow to vital organs and posing an immediate and high risk of death.

what is an aortic aneurysm?

An aortic aneurysm is a bulge or enlargement in the aorta, the large blood vessel that carries oxygenated blood from the heart to the rest of the body. This bulge occurs when the walls of the aorta weaken, and it can be dangerous because the weakened area is at risk of rupturing, leading to severe and potentially life-threatening bleeding.

risk factors for aortic aneurysm

Atherosclerosis

Hypertension

Congenital Weakness; Marfan syndrome

Infection

Trauma

aortic aneurysm in the thoracic area

pain in the

-Back

-Neck

-Substernal

aortic aneurysm in the abdominal area (AAA)

MOST COMMON

-often asymptomatic

-abdominal/ back pain

-palpable if > 4cm (in a thin person)

why are most abdominal aortic aneurysms asymptotic

they often do not cause noticeable symptoms until they become large or rupture

The dilation of the abdominal aorta can occur silently, without causing pain or other noticeable signs, making it challenging to detect without medical imaging

explain the law of Laplace

the Law of Laplace states that larger structures are more prone to rupture because their walls need more strength to withstand internal pressure. This is crucial in understanding the risk of rupture in structures like blood vessels or aneurysms—increased size means increased tension and a higher likelihood of rupture.

explain the law of Laplace continued

increased size (diameter) = increased risk fo rupture

-In the case of an aneurysm, the increase in size is often associated with a weakening of the vessel wall

As the vessel wall weakens, it may balloon or bulge outward, creating an aneurysm. This enlargement is a result of the vessel wall's inability to withstand the normal blood pressure, leading to a localized dilation

how are aortic aneurysms diagnosed

using an ultrasound, CT, or MRI

explain an aortic dissection

acute, LIFE THREATENING hemorrhage into the vessel wall

MOST COMMON IN ASCENDING AORTA

what is an aortic dissection associated with

Trauma; to the chest / Hypertension / atherosclerosis

signs of symptoms of with aortic dissection

abrupt onset serve pain in chest or back, altered pulses upper extremities, syncope “fainting”, hemiplegia/ paralysis

aortic dissection is extremity fatal meaning a

HIGH MORTALITY RATE

-treatment is to control bp & surgery

explore blood pressure management

systolic bp: ventricular contraction

diastolic bp: ventricular relaxation

what is mean arterial pressure (MAP)

mostly done by ICU nurses; and it is a calculation to tell us how well an indivudals is being perfused

-measure of tissue perfusion

what is pulse pressure

the difference (subtraction) between SBP and DBP

short term regulation of BP: NEURAL mechanisms SNS & baroreceptors

Sympathetic nervous system

-increase sympathetic activation; adrenaline(epi) and norepi → vasoconstriction → increased HR → increased contractility = increased cardiac output

^parasymphatic does the same thing but opposite

Baroreceptor (in carotid & aortic arch)

-pressure sensors that keep a constant check on blood pressure

-when pressure is too high, they send a message to the brain to trigger release of ADH

short term regulation of BP: HUMORAL mechanisms SNS & baroreceptors

RAA System

when we have lack of blood flow to the kidneys

RELASE aldosterone: increased sodium and water reabsorption

angiotensin II: VASOCONSTRICTION

ADH

1. osmoreceptors ; increased osmolality

2. baroceptors ; decreased BP

   -increased water reabsorption (kidney) via ADFH

long term regulation of BP

THE KIDNEYS ARE THE MOST IMPORTANT MECHANISM FOR REGULATING BLOOD PRESSURE IN THE LONG TERM

why is renal mechanisms most important

1) regulate BP by regulation fluid volume

2) BP increases → diuresis/ natruresis increases (increase water and sodium excretion

explain what it means by “we think over time people develop high BP because of a ddysregulation of BP by the kidneys”

- a shift in the pressure natriuresis/diuresis relationship is part of the pathophysiology of primary HTN

hypertension = high blood pressure

• affects millions (about 50 million in US)

• two types primary (95%) % secondary

  -primary it is it just happens and we have no real reasoning for it

  -secondary is to it happens because another disease cause it to

the higher the BP, the more risk for

CARDIOVASCULAR PROBLEMS

why is hypertension a “silent disease”

because very rarely does it cause signs and symptoms

-headache, nocturia (need to pee at night), visual disturbances

when do most signs and symptoms occur?

until the organs are damaged

1. Heart → chest pain, MI, heart failure

2. Brain → stroke, TIA

3. Kidney → CKD, failure

4. PAD

5. Eyes → retinopathy

6. Sexual Dysfunction

list risk factors for HTN

Combination of genetics and environment

Family history

Increasing age (generally > 50)

Gender (earlier in men)

African American

Diet: HIGH SODIUM INTAKE; water likes to follow salt

Obesity (central obesity → risk)

Diabetes

Smoking

Excessive dinking of alcohol

what is the pathophysiology of HTN

• vasoconstriction/ increased pressure → remodeling of arterioles/arteries

• key initiation factors

• vasoconstriction/ increased pressure → remodeling of arterioles/arteries

hypertrophy of arterial smooth muscles

permanently narrowed lumen

constant high amounts of pressure will result in a permanently narrowed/constricted lumen

Remodeling of Arterioles/Arteries:

• Response to Stress: The persistent increase in pressure triggers a response in the blood vessels, leading to remodeling.

• Hypertrophy of Arterial Smooth Muscle: The smooth muscle cells in the walls of arterioles and arteries may undergo hypertrophy, which means they increase in size. This is like the muscle cells bulking up in response to the constant stress of increased pressure.

Permanently Narrowed Lumen:

• The reduced lumen size means that there is less space for blood to flow through, contributing to persistent high blood pressure. Additionally, the stiffened and less elastic arteries may not respond as effectively to changes in blood pressure, further exacerbating the hypertension.

what are the key initiating factors

1. dysfunction of SNS, RAA system

2. inflammation & endothelial dysfunction

-loss of normal local vasodilators (ex: nitric oxide)

-increased sensitivity to vasoconstriction

overall in the end: leads to vasoconstriction, increase vascular resistance, renal sodium and eater retention, increase blood volume, and sustained HTN

The combination of increased resistance and volume leads to

sustained high blood pressure (HTN)

consequences of HTN: target organ damage

overtime the the damage that the high amount of pressure can cause on the body

HTN cardiovascular damage

Affects large and small vessels

Accelerated atherosclerosis (high pressure = plaques can develop a lot quicker)

Changes in the myocardium: high systemic vascular resistance, increase workload (afterlod), left ventricle hypertrophy

-can lead to heart failure

hypertension takes a toll on both the large and small blood vessels, accelerates the process of artery blockage, and places additional strain on the heart. This increased workload can lead to changes in the heart's structure and, if left unchecked, may contribute to the development of heart failure

HTN kidney damage

Glomerular damage from vasoconstriction & tissue ischemia

-Hypertension causes the blood vessels in the kidneys to constrict (vasoconstriction) and limits blood supply (ischemia) to certain kidney structures. The glomeruli, which are crucial for filtering waste from the blood, can be damaged in this process.

Nephrosclerosis and chronic kidney disease

-Over time, repeated episodes of vasoconstriction and reduced blood supply lead to nephrosclerosis, a condition characterized by hardening and scarring of the kidney tissue.

• Nephrosclerosis contributes to the progression of chronic kidney disease (CKD), where the kidneys gradually lose their ability to function properly.

Acceleration of diabetic kidney disease

HTN cerebrovascular damage

Risk of stroke, aneurysm, intracranial hemorrhage

• Hypertension puts extra stress on the blood vessels in the brain.

• This increased pressure can lead to different types of damage, including:

  • Stroke: A disruption in blood flow to the brain, often due to a blocked or burst blood vessel.

  • Aneurysm: Weakening and bulging of a blood vessel, which can rupture.

  • Intracranial Hemorrhage: Bleeding within the brain.

Hypertensive encephalopathy (severe case)

• This condition involves brain dysfunction due to rapidly increasing blood pressure.

• Symptoms may include confusion, headaches, and seizures.

HTN retinopathy

Vessels weakened, retinal hemorrhage

• Hypertension can weaken the tiny blood vessels in the retina, the part of the eye that senses light.

• Weakened vessels may rupture, leading to retinal hemorrhage or bleeding in the retina.

Papilledema (optic disc edema)

• High blood pressure can cause swelling of the optic disc, which is the spot where the optic nerve enters the eye.

• This swelling is known as papilledema and can impact vision.

HTN aorta (aneurysms, dissections)

1. Aneurysms:

   • Hypertension puts extra pressure on the walls of the aorta, the largest blood vessel in the body.

   • Over time, this can weaken the walls, leading to the formation of aneurysms—bulging and potentially dangerous enlargements of the aorta.

2. Dissections:

   • Aortic dissections are like tears in the layers of the aorta's wall.

   • High blood pressure can contribute to the initiation and progression of these tears, increasing the risk of aortic dissections.

peripheral arterial disease (PAD)

• Hypertension, or high blood pressure, can contribute to the development and progression of PAD.

• High blood pressure puts extra stress on blood vessels, increasing the risk of atherosclerosis (the buildup of fatty deposits) that leads to PAD.

treatment of primary HTN

LIFESTYLE MODIFICATIONS

-DASH diet of AHA

-weight reduction

-moderate consumption of alcohol

-regular physical exercise

-smoking cessation

PHARMACOLOGICAL treatment of primary HTN

Guidelines on drug selection

Diuretics: decrease blood volume

ACE inhibitors, ARBs: block angiotensin II

Calcium channel blockers: inhibit calcium uptake smooth muscle/cardiac muscle

Beta Blockers: block action catecholamines on heart

Alpha blockers: decrease sympathetic stimulation

hypertensive crisis → urgency

SBP > 180 OR DBP > 120

-with no signs organ damage

they say that they “feel fine”

hypertensive crisis → emergency

high BP with signs od organ dysfunction/ damage

-chest pain, altered LOC, s/s stroke

-progressive organs dysfunction/damage if not treated

hypertensive emergency

ADMIT TO ICU FOR IV THERAPY

-goal to lower SBP 25% in first 2 hours, then to 160100

-rapid reduction can precipitate ischemia due to hypertrophied arteries; thus must be done slowly

secondary HTN

-occurred because of another disease state

1. renal disease (acute or chronic)

-sodium/water retention, HTN

2. renal artery stenosis:

excessive activation RAA system

3. endocrine disorders- Cushings, Hyperaldosteronism

4. Pheochromocytoma

-adrenal medulla tumor produces catecholamines

5. Coarctation of the aorta “defect” in kids: narrowing of the aorta

6. Oral contraceptive drugs

7. Obstructive sleep apnea (not in the book); disruption in breathing can cause high BP

hypertension in children

RATE INCREASING

• Primary HTN risk factors

  -obesity

  -family hx, dyslipidema, type 2 diabetes

• Secondary

  -most commonly d/t renal problems

  -coarctation of the aorta

hypotension is to

low blood pressure

low blood pressure can lead to

inadequate tissue perfusion

Causes: hypovolemia (loosing too much fluid), low cardiac output, severe infection (sepsis = massive vasodilation), antihypertensives (taking too much BP medications, orthostatic

what are signs and symptoms of hypotension

inadequate tissue perfusion / low urine output / diaphoresis (sweating) / increased HR (to compensate for low BP) / dizziness (low blood flow to the brain)

what does systolic blood pressure have to be below in hypotension

< 90 as a guideline

and mean arterial pressure (MAP) > 70: calculation between systolic and diastolic blood pressure

define orthostatic hypotension

when you have a positional change in BP; fall in either diastolic or systolic BP

explain orthostatic hypotension

fall in systolic BP > 20 mmHg & diastolic < 10 mmHG w

-when move to standing position

causes of orthostatic hypotension

often idiopathic (meaning we don’t know)

-but especially common in elderly

Hypovolemia = dehydration

Drug induced (antihypertensives, psych meds)

Bedrest/ immobility: decreased blood volume, vascular tone, weak skeletal muscle

how is orthostatic hypotension diagnosed

via serial BP

-simply take the individuals bp laying down (supine) and then standing up (upright) or tilt table test

orthostatic hypotension treatment

treat cause, safety precautions, caution with antihypertensives

venous circulation

veins don’t have a lot of pressure, since they are volume reservoirs

what is the difference between superficial and deep veins

superficial veins are closer to the skin and deal with blood from the surface, while deep veins are deeper within the body and manage blood from the organs and muscle

-deep veins are usually also BIGGER & really rely on muscle pump to move blood back to heart

explain what are perforator/ connector veins

In simpler terms, perforator veins are like traffic managers, helping blood smoothly move between the visible veins on the skin and the deeper veins within the muscles, ensuring a well-coordinated circulation in our legs.

-in between the different types of veins

purpose of vein valves

to prevent retrograde “backflow” & muscle pump

-we relay heart on both to get blood back to heart

what are varicose veins

dilated, tortuous veins of lower extremities

• Contributing Factos

  Pregnancy

  Obesity (higher intraabdominal pressure)

  ^means more pressure that blood has to work against to get back to the heart^

  Absent/ defective valves

  Prolonged standing; when you stand for a long time, gravity pulls blood downward, making it harder for veins to pump blood back up to the heart.

more common in women

varicose veins explained more

prolonged high pressure → incompetence of valve → venous enlargement → future valve incompetence → increase hydrostatic pressure → edema

In simpler terms, prolonged increased pressure can weaken valves in the veins. Once valves become incompetent, blood pools in the veins, causing them to enlarge. The cycle continues with further valve incompetence and vein enlargement, leading to the development and progression of varicose veins.

signs and symptoms of varicose veins

palpable, tortuous veins, aching, edema

-treatment is elastic stocking; which acts like an extra muscle to try and bring blood back to heart OR close/ remove veins via (sclerotherapy, laser, stripping procedures)

varicose veins are a risk factor for what

chronic venous insufficiency

what is chronic venous insufficiency

veins in the legs struggle to pump blood back to the heart effectively

-tissue congestion; (edema) and increase venous pressure → eventually impaired tissue nutrition

causes of chronic venous insufficiency

Varicose veins

Deep vein thrombosis

Decreased muscle pump (thoes who are on bed rest)

In simple terms, when there's swelling and increased pressure in the veins, it can squeeze the tiny blood vessels that deliver nutrients to tissues. This reduction in blood flow can result in less oxygen and fewer nutrients reaching the tissues, eventually leading to impaired tissue nutrition

→necrosis of subcutaneous tisssue, skin atrophy

Hemosiderin deposit (breakdown RBCs) in tissue → brownish discoloration because of the edema and blow flow RBC are more likely to breakdown in the tissue