Ch 26 and 28 - Disorders of blood flow, blood pressure regulation, and cardiac rhythm

Arteries

carry blood away from the heart

• they have thick, elastic (for stretch and recoil), muscular walls

• have higher pressure

• serve as blood resoviers

Veins

they carry blood to the heart

• they have thinner walls than arteries, but they also have valves

• the pressure in veins is lower

• veins have wider lumen

venuoles are the smallest veins that collect blood from the capillaries and form bigger veins

Capillaries

the smallest BVs that are responsible for gas exchange between blood and interstitial fluid

• connects veins and arteries

Layers of BV wall

1) Tunica Interna → the innermost layer of the BVs, also called the endothelium

• made of simple squamous epithelium

2) Tunica Media → the middle layer made of smooth muscle

• the arteries have more smooth muscle and elastic lamina

3) Tunica Externa → adventitia

Vascular Endothelium

multifunctional tissue that is responsible for

• regulating thrombosis - releases tissue plasminogen activator (t-PA), which helps dissolve blood clots

• controls the transfer of substances - the movement of molecules between the blood and surrounding tissues

• regulates blood flow - release nitric oxide (NO) which relaxes vascular smooth muscle and causes vasodilation

Vascular smooth muscle

regulates blood pressure and systemic vascular resistance

• SNS (sympathetic NS) activation releases norepinephrine (NE), which binds to alpha-1 receptors on vascular smooth muscle - causes vasoconstriction, increased VR and BP

BP

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

• systole → highest during ventricular contraction (120 mmHg)

  • highest pressure, highest sound

• diastolic pressure → sustained pressure during ventricular relaxation (80 mmHg)

• pulse pressure (PP) → difference between systolic and diastolic blood pressure

Factors that alter BP

1) Cardiac Output (CO) → volume of blood pumped by the ventricle per minute

2) Blood Volume → total amount of blood circulating in the body

• increased blood volume - increases CO and BP

• decreased blood volume - decreases CO and BP

CO = BP

BV = BP

CO = BV

3) Blood vessel diameter (peripheral resistance) → vasoconstriction increases pressure and resistance; vasodilation decreases pressure and resistance

Short term pressure regulation

managed by the sympathetic NS

• SNS regulates BP rapidly by adjusting heart activity and blood vessel diameter

blood pressure regulation

Baroreceptor reflex

primary neural mechanism for short-term BP regulation

• works through a negative feedback loop involving pressure sensors and the ANS (autonomic)

if the body senses increased blood pressure, the baroreceptor reflex will work to decrease the blood pressure (and vice versa)

Barorecptors

stretch-sensitive receptors located in the walls of the carotid sinuses and aortic arch

• they detect BP changes and signal the brain to adjust HR, CO, and BV diameter

Hormonal Regulation of BP

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

• involves ADH, renin-angiotensin-aldosterone system (RAAS), and epinephrine

antidiuretic hormone (ADH)

increases water reabsorption by the kidneys, raises blood volume and blood pressure

Renin-angiotensin-aldosterone systen (RAAS)

is activated when BP, BV, and kidney perfusion decreases

raises BP through vasoconstriction and increased sodium and water retention

Epinephrine

increases HR and cardiac contractility and can cause vasoconstriction

RAAS Pathogenesis

1. RAAS is stimulated by low blood pressure, this causes the juxtaglomerular cells in the kidneys to release renin

2. Renin stimulates the conversion of angiotensinogen into angiotensin I

3. Angiotensin I enters the lungs and is converted by converting enzymes into angiotensin II

4. Angiotensin II causes two things: vasoconstriction on the arterioles and stimulates aldosterone release by the pituitary gland (causing sodium and water retention in the kidneys)

5. this increases BV and BP

Lipoproteins

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

1. chylomicrons - transport dietary triglycerides

2. VLDL - transports triglycerides synthesized in the liver

   1. mainly made of triglycerides, 10% cholesterol, and 5-10% proteins

3. LDL - the main carrier of cholesterol

4. HDL - 50% protein (has increased protein and decreased cholesterol)

   1. made of 5% triglycerides, 20% cholesterol, and 50% proteins

LDL and HDL are important for cardiovascular health

Low Density Lipoproteins (LDLs)

“bad” cholesterol

• transports cholesterol from the liver to the body cells (tissues)

• high LDL lvls contribute to athroma (plaque) formation

High-Density Lipoprotein (HDL)

“good” cholesterol

• transports cholesterol from the tissues to the liver for breakdown and excretion of bile

• cholesterol is broken down or converted into bile acids and can be eliminated through bile and feces

• helps remove excess cholesterol from tissues and support cardiovascular health

Hypercholesterolemia (+ primary and secondary)

high level of cholesterol in the blood

• total serum cholesterol lvl of 240 mg/dL or higher

• contributes 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 (DM), obesity, and hypothyroidism

Arteriosclerosis

general term for the thickening, hardening, and loss of elasticity of the arteries

• arteries become still, making it harder to maintain normal blood flow

Atherosclerosis

type of arteriosclerosis characterized by the buildup of fatty plaques called atheromas in the walls and medium-sized arteries

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

• plaque generally narrow the arterial lumen and may restrict or block blood flow (causing ischemia, maybe rupture and become emboli)

Pathogenesis of Atherosclerosis

1. endothelial injury → dmg to the endothelium triggers an inflammatory response

2. LDL enters and accumulates in the dmged arterial wall

3. LDL becomes oxidized, promoting inflammation and free radical formation

4. endothelial cells release inflammatory chemicals (monocytes and T lymphocytes) that attract immune cells to the affected area

5. macrophages engulf oxidized LDL cholesterol and become foam cells

6. smooth muscle cells migrate and multiply within the arterial wall - forms a fibrous cap over the fatty core

Atherosclerotic Plaque

complete plaque that contains a CAP

• the cap has smooth muscle and fibrous tissue

• the shoulder area is weak!!!

Stable Plaques

have a 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

Unstable Plaques

have thin fibrous caps

• more likely to rupture or erode

• can trigger rapid blood clot formation

• may completely block the artery or become an embolus

Non-modifiable factors vs Modifiable factors

non-modifiable factors - cannot be changed

• age → risk for atherosclerosis increases as people get older

• genetic/familial factors → family history and inherited conditions can increase risk

modifiable factors - can be reduced or manageable

• obesity and sedentary life-style - increases the risk of hypercholesterolemia

• cigarette smoking

• diabetes mellitus

• poorly controlled HTN

Progression of Atherosclerosis

it progresses as lipids accumulate in the arterial wall, inflammation develops, and plaques become more complex

• fatty streaks are the earliest visible lesion; they appear as thin, flat, yellow discolorations in the intima that progressively enlarge (initially very small)

• fibrous atheromatous plaque develop as lipids accumulate and fibrous cap forms over the lipid core; gradually thickens and narrows the arterial lumen

• complicated lesion is an advanced and more complex atherosclerotic plaque that may rupture and cause ulceration, hemorrhage, and blood clot

complicated lesion can cause development of a thrombus that can completely grow or block blood flow

What arteries are more frequently involved with atherosclerosis

arteries suppling the heart, brain, kidneys, lower extremities, and small intestines

• in larger arteries, like the aorta, the common complications are thrombus formation and weakening of the vessel wall - can lead to aneurysm

• in medium sized arteries (the carotid), ischemia and infraction due to vessel occlusion are more common

look at slide 29

Peripheral Arterial Disease

the narrowing or blockage of the arteries supplying the lower extremities due to atherosclerotic plaque buildup

• common cardiovascular condition — approx. 21 million americans aged 40 and older are affected by the disease

• is initially asymptomatic: PAD may cause no noticeable symptoms until blood flow becomes significantly reduced (when 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, although this is uncommon

PAD Manfiestations

intermitten claudication

• leg pain or cramping during walking or exercise that improves with rest

• the gastrocnemius muscle requires increased oxygen during exercise

• narrowed arteries limit blood flor and oxygen delivery, causing ischemic pain (ischemic stimulates nerve endings)

advanced symptoms - sever arterial narrowing or occlusion can cause reduced blood flow even at rest (absent or diminished pulse)

• pain in the legs or feet as rest, weak distal pulse

• redness in the depended position due to gravity

• thinning of skin, non-healing sores, nail changes

Treatment of PAD

• walking slowly

• avoid injury

• anti-platelet agents

• bypass grafting

• angioplasty

  • angioplasty is a less invasive treatment than bypass, happens when a catheter is inserted

  • if this doesn’t work, they then have to do a bypass

Acute Arterial Occlusion

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

• manifestations: the 5 P’s (not all the symptoms need to be present simultaneously for there to be acute arterial occlusion, but the present of 5 means there is an occlusion)

  • pistol shot (acute) → sudden, severe pain

  • pulselessness → absence of a palpable pulse

  • paralysis → muscle weakness

  • paresthesia → burning, numbness

  • pallor → pale skin

  • polar → cold skin

Thromboangitis obliterans (TAO) (also called buerger’s disease)

rare, progressive, non-atherosclerotic inflammatory disease that affects small and medium sized blood vessels

characterized by -

• inflammation - BVs become inflamed and swollen

• narrowing and occlusion → inflammation causes the vessels to narrow and become blocked by blood clots (thrombosis)

• reduced blood flow → the blockage severely reduced blood flow to the fingers, toes, hands, and feet

more commonly affects men >45 years and older

manifestations of TAO

early symptom - pain at rest

affects the plantar and digital vessels in the foot - causes ischemic ulcerations and gangrene

Aneurysm

localized dilation and weakening of an arterial wall that is often associated with damage to the middle layer (tunica media)

• common in larger and medium sized arteries

Saccular Aneurysm

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

Fusiform aneurysm

circumferential dilation along a section of artery

Dissecting aneyrism

occurs when a tear develops in the inner arterial layer (tunica intima), allowing blood to enter and separate the layers of the arterial wall (more severe, causes bleeding inside the arteries)

Berry Aneurysm

commonly occurs in the circle of willis in the brain

• consists of a small, spherical vessel dilation

Fusiform and Saccular Aneurysms

commonly occur in the thoracic or abdominal aorta

• characterized by gradual and progressive enlargement of the aorta

Abdominal aortic aneurysm

the wall of the aorta weakens and stretches

• frequently asymptomatic; there is a risk for clot formation, rupture, and hemorrhage

• common hear bruit with stethoscope (may be heard over affected artery due to turbulent blood flow)

• pulsating abdominal mass (may be felt during palpation, requires evaluation)

Dissecting Aneurysm

hemorrhage occurs, forms a blood-filled channel

• dmg to the inner layer of the aorta allowing blood to enter the space and separate the layers of the arterial wall

• more common in men aged 40-60 w/ history of HTN

clinical manifestations

• abrupt excruciating pain - described as ripping or tearing chest or back pain

• BP and pulse unobtainable

• high mortality risk - severe internal bleeding, and death without immediate treatment

Varicose Veins

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

• faulty valves allow blood to flow backward and accumulate in the veins (valves in deep leg veins do not close completely)

  • this increases venous pressure, causing the veins to enlarge and become twisted

  • appear as irregular, purplish, bulging structures in the legs

• risk factors - familial tendency, high BMI, and parity (?)

Thrombophelbitis

inflammation of the vein associated with formation of a blood clot

• signs and symptoms:

  • may be asymptomatic or go unnoticed

  • aching or burning sensation

  • tenderness, redness, and swelling around the affected vein

• serious risk of pulmonary embolism → obstruction of pulmonary arteries by emobli

Virchow’s Triad

three major factors that increase the risk of venous thrombosis

• venous stasis → sluggish or reduced blood flow causing a buildup of blood in the veins

• endothelial injury → any injury can initiate blood clotting

• increased blood coagulability

HTN

high blood pressure, common in any age group

• BP reading of 130/88 mmHg or higher is HTN

• frequently asymptomatic in stage 1 (early stages)

• when present, symptoms can be vague and nonspecific, like fatigue and morning occipital headache

Primary (essential) HTN

most common type of HTN

• develops gradually over many years with no identifiable cause

• pathophysiology mechanism: increase in SNS activity causes

  • arteriolar vasoconstriction → increases total peripheral resistance (TTR)

  • increased HR and cardiac contractibility → can increase cardiac output (CO)

  • stimulation of the RAAS → promotes sodium and water retention, increasing blood volume

    • activated because of vasoconstriction of arteries supplying kidneys

Secondary HTN

high blood pressure caused by an identifiable underlying condition

• common causes:

  • renal disease → kidney disorders that affect fluid balance and BP regulation

  • endocrine disorders → hormonal imbalances that increase BP

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

Malignant HTN

severe, rapidly progressive form of HTN that can cause acute dmg to vital organs

• extremely elevated BP, often with diastolic pressure around or above 120 mmHg

• can cause serious complications involving the brain, heart, kidneys, and eyes

Left ventricular hypertrophy (LVH)

when the left ventricle wall thickens due to the heart having to work harder to pump blood against increased vascular resistance (increased afterload)

• the heart wall becomes thicker leaving less room for ventricular filling and less efficient pumping, leading to heart failure

complication of HTN

Nephrosclerosis

dmg and hardening of small renal BVs due to long-standing HTN

• complication of HTN

Glomerular dmg

reduced blood supply and injury to the glomeruli

• complication of HTN

Stroke

HTN damages and weakens the cerebral BVs, increasing the risk of ischemic and hemorrhagic stroke

Predisposing factors of HTN

• age → increases with age

• sex → men tend to develop HTN earlier in life, women around middle age/after menopause

• genetic factors → familial history and inherited predisposition

• high sodium intake → excess salt can increase blood pressure

• smoking → damages BVs and increases cardiovascular risk

• chronic stress → prolonged or recurrent stress may contribute to elevated BP (the #1 predisposing factor)

Management of HTN

• reduced sodium (salt) intake

• achieve and maintain a healthy body weight

• reduce stress

• drug therapy → ACE inhibitors, calcium channel blockers, diuretics

Cardiac Conduction System

groups of specialized cells that conduct and transmit electrical impulses

• sinoatrial (SA) node → natural pacemaker of the heart (60-100 APs in one minute)

  • initiates the electrical impulse, setting the heart rate at rest to about 60-100 BPM in adults

• atrioventricular (AV) node → briefly delays the impulse, allowing the ventricles to fill with blood before they contract

• Bundle of His (AV bundle) → carries the impulse from the AV node

• R and L bundle branches → conducts electrical impulses down the interventricular system

• Purkinje Fibers → spread the impulse rapidly throughout the ventricular muscle

electrocardiogram (ECG)

test that records the electrical activity of the heart and is used to assess rhythm, heart rate, and abnormalities in electrical conduction

Waves Segments and Intervals of a normal ECG

P wave → atrial depolarization (contraction)

QRS wave → ventricular depolarization (contraction)

T wave → ventricle depolarization (relaxation)

P-R interval → beginning of atrial excitation to beginning of ventricular excitation

S-T segment → entire ventricular myocardium depolarized (shows ventricular ejection)

Q-T interval → beginning of ventricular depolarization through ventricular depolarization

Heart rate

number of heart contractions (beats) per minute

• on ECG measure distance between two consecutive R waves (RR interval)

H

Heart Rythym

pattern and regularity of the heart’s electrical activity

Arrhythmias

deviations from normal cardiac rate of rhythm, caused by disturbances in the heart’s electrical conduction system

• some are caused by reduction of the efficiency of the heart’s pumping cycle

• electrocardiography - used to monitor the heart’s electrical activity and conduction system; helps detect abnormal HRs, irregular rhythms, and conduction disturbances

SA node

pacemaker of the heart that give the heart its normal resting rate of 60-100 bpm in adults

Bradycardia, tachycardia, and sick sinus syndrome

bradycardia → regular but slow heart rate below 60 bpm

tachycardia → regular but fast heart rate above 100 bpm

sick sinus syndrome → alternating episodes of fast and slow heart rhythms - tachy-brady syndomre

premature atrial contractions

extra contraction or ectopic beats due to irritable atrial muscle cells outside conduction pathway

atrial flutter

atrial heart rate of 160 to 350 beats/min

• AV node delays conduction — ventricular rate is slower

atrial fibrillation

atrial rate over 350 beats/min ventricular rate slower

• causes pooling of blood in the atria — thrombus formation is at risk

heart block

electrical impulse traveling from the atria to the ventricles are delayed or completely blocked, usually at the AV node or below i

first-degree AV block

electrical impulses are delayed, but all impulse reach the ventricles

• ECG - PR interval is longer than .20 seconds

• often causes no symptoms

second-degree block

every second to third atrial beat dropped at AV node causing slower rate or irregular heart rhythm - progressive long PR

• not every signal developed at AV node is reaching

third degree block

no transmission from atria to ventricles

• normal atrial rate, ventricular rate is 30-40 bpm

bundle branch block

interference with conduction in on of the bundle branches

• right bundle branch block - electrical conduction through the right bundle branch is delayed or blocked

• left bundle branch block - electrical conduction through the left bundle branch is delayed or blocked

the left and right ventricles contract asynchronously

ventricular tachycardia

ventricular rate 100-200 bpm

• likely to reduce CO as reduced diastole occurs (the ventricles have less time to fill up with blood)

ventricular fibrillation

muscle fibers contract independently and rapidly, no CO

• no identifiable, organized P waves or QRS complex

• cardiac standstill (asystole) occurs if not treated immediately

premature ventricular contractions

additional ectopic beats

• may induce fibrillation