Chapter 26 Disorders of Blood Flow and Blood Pressure Regulation

Chapter 26: Disorders of Blood Flow and Blood Pressure Regulation

Dr. Kelly Goebel DNP, ACNP-BC

Page 1: Overview

  • Focus on disorders affecting blood flow and blood pressure regulation.

Page 2: Vascular Structure

  • Components of Blood Vessels:

    • Collagen and internal elastic fibers

    • Smooth muscle cells

    • Connective tissue

    • Endothelial cells

    • Lumen

    • Tunica externa, tunica media, tunica intima

Page 3: Structure and Function

  • Endothelium→ single layer of cells

    • Controls vascular function, platelet adhesion, blood clotting, blood flow modulation, immune regulation.

    • Dysfunction caused by inflammation, hemodynamic stress, lipid molecules, hypoxia.

    • Releases cytokines and growth factors, influencing nitric oxide (relaxing) and endothelin (contracting).

  • Vascular Smooth Muscle Cells (SMCs):

    • Located in tunica media, respond to hormonal and neural stimulation to constrict/dilate blood vessels.

Page 4: Function of Blood Vessels

  • Arterioles:

    • Narrow lumen, regulates blood pressure via vasoconstriction/dilation.

  • Arteries:

    • Transport blood from heart to organs; no exchange of substances.

  • Capillaries:

    • Site of exchange for fluids, gases, nutrients; highly permeable.

  • Veins:

    • Transport blood back to heart; larger diameter, valvular structures prevent backflow.

  • Venules:

    • Collect fluid from capillaries; larger than capillaries, valves present.

Page 5: Blood Pressure Dynamics

  • Systole: - contraction

    • Blood pressure rises during left ventricle contraction.

  • Diastole:- Relaxation

    • Blood pressure falls as the heart relaxes.

Page 6: Regulation of Systemic Arterial Blood Pressure

  • Systolic Pressure: < 120 mm Hg

  • Diastolic Pressure: < 80 mm Hg

  • pulse pressure= systolic- diastolic

  • Mean Arterial Pressure (MAP):

    • Average pressure during ventricular contraction/relaxation; indicator of tissue perfusion (90-100 mm Hg).

Page 7: Mechanisms of Blood Pressure Regulation

  • Key Factors:

    • Cardiac output, peripheral vascular resistance, sympathetic activity, stroke volume, heart rate.

  • Hormonal Influences:

    • Angiotensin II, aldosterone, and the renin-angiotensin mechanism.

Page 8: Neural Regulation

  • Vagal Nerve Stimulation: Causes bradycardia. (rectal pressure stimulates vagal never)

  • Sympathetic Stimulation: Causes tachycardia.

  • Baroreceptors: Pressure-sensitive receptors (in the walls of blood vessels) affecting heart rate and vascular tone.→ contraction and heart rate increase

Page 9: Hormonal Regulation

  • Renin-Angiotensin-Aldosterone System (RAAS):

    • Involves angiotensinogen, renin, angiotensin I, and II, leading to vasoconstriction and sodium reabsorption→ increasing BP

Page 10: Systolic Blood Pressure Factors

  • Reflects:

    • Blood volume ejected, rate and force of ejection, elasticity of arteries.

    • Stroke volume = Volume of blood ejected from the ventricles with each beat

    • Cardiac output= SVx HR

Page 11: Diastolic Blood Pressure Factors

  • Reflects:

    • Closure of aortic valve, energy stored in elastic fibers, resistance to flow through arterioles.

Page 12: Disorders of Systemic Arterial Blood Flow

  • Impact of Arterial Disease:

    • Impairs blood flow, leading to ischemia (insufficient oxygen) and infarction (necrosis due to occlusion) → dead tissue within a living organism

Page 13: Dyslipidemia

  • Definition: Imbalance of lipid components in blood.

  • Types:

    • Hyperlipidemia(cholesterol, triglycerides, phospholipids), hypercholesterolemia, hypertriglyceridemia.

  • Lipoprotein Classifications:

    • VLDL, LDL (atherogenic)→ carry to the tissues, HDL (protective)→ remove to the tissue and take it to the liver

Page 14: Risk Factors for Dyslipidemia

  • Primary: Genetic basis (familial hypercholesterolemia).

  • Secondary: Dietary factors, obesity, Type II Diabetes, metabolic syndrome ( high glucose, BP, waist circunfe)

Page 15: Atherosclerosis

  • Definition: Formation of fibrofatty lesions in arteries.

  • Major Risk Factor: Hypercholesterolemia.

  • Traditional and Modifiable Risk Factors: Smoking, obesity, hypertension, diabetes.

  • screening risk: elevated CRP levels (c reactive protein -levels of inflammation)

Page 16: Pathogenesis of Atherosclerosis

  • Lesions:

    • Fatty streaks, fibrous atheromatous plaque(accumulation of lipid, proliferation of vascular smooth muscle cells, formation of scar tissue), complicated lesions, gets bigger→hemorrhage, ulceration)

  • Impact on Artery Lumen: Decreases as lesions grow.

Page 17-20: Development of Atherosclerosis

  • Stages:

    • Endothelial injury→ monocytes/ platelets adhere

    • inflammatory cell migration→monocytes into macrophages.

    • lipid accumulation→ Foam cells accumulation (macrophages that engulfs lipoproteins), necrotic debri in celular wall

    • plaque structure formation→ aggregation of macrophages, leukocytes, collagen→ formation of fibrous cap

Page 21: Clinical Manifestations of Atherosclerosis

  • Effects:

    • Ischemia, vessel obstruction, thrombosis, aneurysm formation(vessel weakening).

  • Commonly Affected Areas: Heart, brain, kidneys, lower extremities.

Page 22-24: Aneurysms

  • Definition: Abnormal localized dilation of blood vessels, most common in the aorta.

  • Etiology: Congenital, trauma, infection, atherosclerosis, elevated lipids, hypertension, smoking

  • Clinical Manifestations: Vary by size and location.

    • Thoracic

    • Abdominal (pulsating mass,

  • Classification: Ascending, arch, descending, thoracoabdominal, abdominal.

Page 25-26: Aortic Dissection

  • hemorrhage into vessel wall w/ tearing

  • Etiology: Hypertension, degeneration of medial layer of vessel wall

  • Clinical Manifestations of Dissection: Severe chest pain(tearing or ripping), elevated BP(will become unobtainable in one or both arms as the dissection disrupts arterial flow to arms) , potential for syncope,paralysis, and heart failure.

Page 27-30: Acute Arterial Occlusion

  • Etiology: Sudden interruption of arterial flow due to

    • embolus(is a thrombus piece that can travel in the body)→atrial fibrillation can cause emboli and make it travel in the body, ischemic heart; Emboli can lodge in major arteries

    • thrombus

  • Clinical Manifestations(6Ps): sudden onset of Pallor, pain, pulselessness, paresthesia(numbness, tingling) , paralysis, cold extremities.


Atherosclerotic Occlusive Disease (chronic occlusive arterial)

  • Common in lower extremity (femoral/popliteal)

  • Etiology:

    • advanced age

    • smoking

  • Manifestation

    • gradual

    • claudication (pain w/ walking) Calf pain

    • weak pedal pulses

    • ischemic pain at rest, ulceration, gangrene, tissue necrosis

Page 31-34: Disorders of Systemic Venous Circulation

  • Thromboembolism: Presence of thrombus in veins+inflammation,

    • Etiology - Virchow’s Triad

      • stasis of blood

      • hypercoagulability- Factor V Leiden

      • vessel wall injury

    • Manifestation- Pain, swelling(calf, posterior tibial), deep muscle tenderness, sometimes asymptomatic

  • Chronic Venous Insufficiency: Persistent venous hypertension leading to tissue congestion:edema and skin changes(brown pigmentation, stasis dermatitis →thin , shinny, bluish brown, irregularly pigment skin)

    • Etiology: prolonged standing, incompetent valves, DVT, inflammation, endothelial dysfunction.

    • Stages→ spider veins, varicose, swelling, skin changes, venous ulcer

Page 35-40: Disorders of Blood Pressure Regulation

  • Importance of Regulation: Ensures adequate tissue perfusion and prevents vessel damage.

  • Low BP→ don’t receive suff blood- don’t receive nutrients, oxygen and cell wate removal - hypoxic ischemia

  • HIgh BP- damage endothelial tissue, risk o atheosclerotic vascular disease and vascular rupture

  • Hypertension:

    • Primary: No specific cause; risk factors include genetics, age, gender, race, family history. modifiable- dietary, tobacco, obesity, diabetes

    • Secondary: Caused by medical conditions (e.g., renal failure). cocaine

  • Clinical Consequences: increase workload in LV hyperplasia(bc the the vessel is too vasoconstricted)

    • Blindness, chronic kidney disease, stroke, angina(chest pain), AMI,

  • Target organ damage, including heart, brain, kidneys, and vision.

  • Classification Guidelines: Based on systolic and diastolic blood pressure readings.