What is stroke volume, peripheral vascular resistance, Cardiac output, Blood Pressure

• Stroke volume refers to the amount of blood ejected from the heart with each beat
• Total peripheral resistance refers to radius of arterioles + viscosity of blood:
  
  • Peripheral resistance Increases If
    • Increased blood viscosity
    • Reduction in the size of arterioles
• Cardiac output (CO) = heart rate × stroke volume
• Blood pressure (BP) = cardiac output × total peripheral resistance

HDL

Synthesis & Function?

• HDL is synthesized in:
• Liver
• Intestine

• HDL helps to remove excess cholesterol from tissues and other lipoproteins
• Excess cholesterol from the other lipoproteins are transferred to HDL thereby increasing HDL mass

HTN

What are different types of HTN?

Increases the risk for what?

Hypertension

• Consistent elevation of systemic arterial blood pressure
• Sustained elevation of 130 mmHg systolic or higher OR 80 mmHg diastolic or higher

Isolated systolic hypertension: elevated systolic blood pressure accompanied by normal diastolic blood pressure

Primary (essential) hypertension

• Genetic and environmental factors
  

Secondary hypertension

• Is caused by altered hemodynamics from an underlying primary disease or drugs (i.e.. pheochromocytoma, renal artery stenosis, Cushing’s, primary hyperaldosteronism). Only 5-10% of all HTN

• Affects the entire cardiovascular system
• Systolic hypertension: most significant factor in causing target organ damage
• Increases the risk for myocardial infarction (MI), kidney disease, and stroke

HTN Causes

• Caused by
• Increases in cardiac output or total peripheral resistance, or both
• Cardiac output increased: any condition that increases heart rate or stroke volume
• Peripheral resistance increased: any factor that increases blood viscosity or reduces vessel diameter (vasoconstriction)

Causes of Secondary HTN

• renal vascular or parenchymal disease
• adrenocortical tumors
• adrenomedullary tumors (pheochromocytoma)
• drugs (oral contraceptives, corticosteroids, antihistamines)

Corticosteroids cause the body to retain fluid. Extra fluid in the circulation can cause an increase in blood pressure

oral contraceptives cause changes in the renin-angiotensin-aldosterone system, particularly a consistent and marked increase in the plasma renin substrate concentrations

Causes of HTN in older adults

• High blood pressure is more common in older adults for multiple reasons:
• Large arteries stiffen
• Baroreceptor sensitivity is decreased
• Peripheral vascular resistance is increased
• Renal blood flow is decreased

Primary HTN Patho

Multiple pathophysiologic mechanisms mediate these effects including the sympathetic nervous system (SNS), the RAAS, and natriuretic peptides.

• Overactivity of the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS), and alterations in natriuretic peptides
• Inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance

HTN Risk Factors

Non Modifiable

• Positive family history
• Advancing age
• Gender: female >70 years of age; male <55 years of age
• Race: Black
• Glucose intolerance (diabetes mellitus)/insulin resistance)

Modifiable

• Heavy alcohol use
• Obesity
• Cigarettes
• ↑Sodium (Na+) intake
• ↓Potassium (K+), magnesium (Mg++), calcium (Ca++) Low levels of dietary
  potassium, calcium, and magnesium also are risk factors because
  sodium is retained without their intake.

Nicotine stimulates the release of
catecholamines (epinephrine and norepinephrine), which increases
heart rate and causes peripheral vascular constriction. As a result
blood pressure increases, as do cardiac workload and oxygen
demand. Cigarette smoking is associated with an increase in LDL and
a decrease in HDL levels, and contributes to vessel inflammation and
thrombosis.

These effects can include endothelial damage, thickening of the vessel
wall, increased inflammation and leukocyte adhesion, increased
thrombosis, glycation of vascular proteins, and decreased production
of endothelial-derived vasodilators such as nitric oxide96

HTN S/S

KNOWN AS THE SILENT DISEASE =

• Early stages of hypertension have no clinical manifestations other than elevated blood pressure.

Most clinical manifestations of hypertensive disease are caused by
complications affecting the target organs. Evidence of heart disease,
renal insufficiency, central nervous system dysfunction, impaired
vision, impaired mobility, vascular occlusion, or edema can all be
caused by sustained hypertension

HTN Diagnosis

Diagnosis

• Measurement of blood pressure on at least two separate occasions averaging two readings at least 2 minutes apart with the individual seated, the arm supported at heart level, after 5 minutes of rest, with no smoking or caffeine intake in the past 30 minutes

HTN Treatment

Treatment

• Reducing or eliminating risk factors
• Dietary approaches to stop hypertension (DASH diet)
• Cessation of smoking
• Exercise program that promotes endurance and relaxation

Medications

• Pharmacologic therapies
• Angiotensin-converting enzyme (ACE) inhibitors
• Angiotensin-receptor blockers (ARBs)
• Calcium channel blockers
• Combination of thiazide diuretics and other antihypertensives
• Aldosterone antagonists
• Beta blockers

Orthostatic Hypotension

What is it?

An abnormal drop in blood pressure that occurs when a person stands after having been in the seated or supine position.

Orthostartic Hypotension Patho

When a person stands and there is an absence of normal circulatory reflexes (e.g. baroreceptor response) or blood volume, blood then pools in the lower body. --> This thereby causes: decreased cardiac output, decreased blood pressure, and decreased blood flow to the brain

Causes of Orthostatic hypotension

Medications

Prolonged immobility

Aging effects on postural reflexes

Diagnosis of Orthostatic HTN

Defined as at least 20mmHg drop in systolic blood pressure or 10mmHg drop in diastolic blood pressure within 3 minutes of standing.

Orthostatic Hypotension S/S

lightheadedness, syncope, or both.

What is Astherosclerosis?

Leading cause of ?

A medical condition in which the artery wall thickens as a result of the accumulation of fatty materials

• Atherosclerosis is a leading cause of:
• Coronary artery disease
• Stroke
• Peripheral vascular disease

What are 4 steps of development of athersclerosis?

1. Endothelial Cell Injury
2. Migration of Inflammatory Cells
3. Lipid Accumulation and Smooth Muscle Cell Proliferation
4. Plaque Structure

What happens in Endothelial Cell Injury?

What are injury agents?

• The vascular endothelium is injured by agents, causing monocytes and platelets to adhere to the endothelium
• The injurious agents may be:
• smoking
• elevated LDL
• hypertension
• inflammatory mediators

What happens in Migration of Inflammatory Cells?

Monocytes migrate to the intima where they become macrophages and engulf LDL

What happens in Lipid Accumulation and Smooth Muscle Cell Proliferation

• Activated macrophages release free radicals causing oxidation of LDL
• The macrophages ingest the oxidized LDL which results in forming foam cells (the primary component of atherosclerotic lesions)
• Activated macrophages also produce growth factors that contribute to proliferation of smooth muscle cells

What happens in Plaque Structure?

• Atherosclerotic plaques consist of an aggregation of:
• smooth muscle cells
• macrophages
• other leukocytes
• There are both intracellular and extracellular lipids
• The fibrous cap is made of smooth muscle cells and extracellular matrix (collagen + elastic fibers).
• Below the fibrous cap is a central core of lipid-laden foam cells and fatty debris.

• **Rupture, ulceration, or erosion of an unstable or vulnerable fibrous cap may lead to hemorrhage into the plaque. Or a thrombotic occlusion of the vessel lumen

What is varicose veins?

• Vein in which blood has pooled
• Distortion, leakage, increased intravascular hydrostatic pressure, and inflammation of veins
• Increases risk for clotting, DVT

Varicose veins Causes

Varicose veins prevention?

Varicose veins treatment?

Causes

• incompetent valves, venous obstruction, muscle pump dysfunction, or combination of these.

Prevention

• healthy weight, exercise, avoid standing for long periods of time, smoking cessation, support hose

Treatment

• Ablation, Sclerotherapy, Surgery

Peripheral Artery Disease: Clinical Presentation

• The principal sign of chronic obstructive arterial disease is pain while walking (aka claudication).
• The gastrocnemius muscle of the calf consumes the most oxygen of any muscle in the leg when walking
• Calf area is where patients with PAD complain of pain

• When blood flow is severely diminished, pain may occur at rest (not just walking) due to the ischemia.
• Over time, ulceration and gangrene may occur.

PAD S/S of chronic ischemia

Other signs of chronic ischemia include:

• Atrophy and thinning of the skin in the lower leg
• Decreased size of leg muscles
• Cool feet
• Popliteal and pedal pulses are weak or absent

What is peripheral artery disease?

Risk Factors?

• Atherosclerotic disease of arteries that perfuse limbs, especially lower extremities
• Risk factors
• Smoking
• Hypertension
• Hyperlipidemia
• Diabetes

Peripheral Artery Diagnositics

• Patients with peripheral arterial disease (PAD) often have weak or absent pulses.
• Palpating by hand for these pulses is difficult ---> using doppler ultrasound stethoscope may be used for both detecting the pulses and measuring of blood pressure.
• Ankle-brachial index (ABI) is the ratio of the systolic blood pressure from either the dorsalis pedis or posterior tibial artery to the systolic blood pressure obtained from the brachial artery.
  • Normal ABI range is 1.0-1.4
  • ABI of 0.9 or less indicates PAD

• Ankle-brachial index (ABI) Values Normal & PAD

• Brachial Systolic BP/Ankle systolic BP
• Normal ABI range is 1.0-1.4
• ABI of 0.9 or less indicates PAD

Peripheral Artery Disease Treatment

Treatment

• Vasodilators
• Antiplatelet or antithrombotic medications (e.g., aspirin, cilostazol, ticlopidine, clopidogrel)
• Cholesterol-lowering medications
• Exercise rehabilitation

Deep Vein Thrombosis What is it?

Three main risk factors?

• Deep venous thrombosis (DVT)
  • Clot in a large vein
  • Obstruction of venous flow leading to increased venous pressure
• Thrombosis: clot
• Detached thrombus: thromboembolus; can lead to pulmonary emboli

• Factors: Virchow triad
  • Venous stasis
  • Venous intimal damage
  • Hypercoagulable states

Deep Vein Thrombisis S/S

Clinical Manifestations

• Pain, swelling, redness of affected limb
• (Homan’s sign is not a reliable test for DVT. It is neither specific or sensitive for DVT)

DVT Prevention

Prevention is crucial

• Mobilization soon after surgery, illness, injury
• Prophylactic low–molecular-weight heparin or direct thrombin inhibitors

DVT Diagnostic Test & Treatment

Tests

• D-dimer and Doppler

Treatment

• Low–molecular-weight heparin
• Direct thrombin inhibitors
• Aspirin therapy
• Catheter directed thrombolytic therapy