Vascular Disease Hypertension Disorders of Cardiac Function
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  • Xanthomas in skin or tendonsArcuslipoides
  • FIGURE 22-7 • Fibrofatty plaque of atherosclerosis. (A) In this fully developed fibrous plaque, the core contains lipid-filled macrophages and necrotic smooth muscle cell debris. The “fibrous” cap is composed largely of smooth muscle cells, which produce collagen, small amounts of elastin, and glycosaminoglycans. Also shown are infiltrating macrophages and lymphocytes. Note that the endothelium over the surface of the fibrous cap frequently appears intact. (B) The aorta shows discrete raised, tan plaques. Focal plaque ulcerations are also evident. (From Gotlieb A. I. [2005]. Blood vessels. In Rubin E., Gorstein F., Rubin R., et al. [Eds.], Pathology: Clinicopathologic foundations of medicine [4th ed., p. 487]. Philadelphia: Lippincott Williams & Wilkins.)
  • Anti NeutrophilCytoplasmic Antibodies
  • CCB Calcium Channel Blocker, Prazosin (alpha blocker)
  • Cause unknown, autoimmune suggestion, 10% Risk of aortic anuerysm
  • Temporal arteritis. A cross-sectional photograph of a temporal artery shows inflammation throughout the wall, giant cells (arrow), and a lumen severely narrowed by intimal thickening. (From Gotlieb A. I. [2005]. Blood vessels. In Rubin E., Gorstein F., Rubin R, et al. [Eds.], Pathology: Clinicopathologic foundations of medicine [4th ed., p. 507]. Philadelphia: Lippincott Williams & Wilkins.)
  • Three forms of aneurysms: (A) berry aneurysm in the circle of Willis, (B) aortic dissection, and (C) fusiform-type aneurysm of the abdominal aorta.
  • FIGURE 22-11 • Atherosclerotic aneurysm of the abdominal aorta. The aneurysm has been opened longitudinally to reveal a large thrombus in the lumen. The aorta and common iliac arteries display complicated lesions of atherosclerosis. (From Gotlieb A. I. [2005]. Blood vessels. In Rubin E., Gorstein F., Rubin R., et al. [Eds.], Pathology: Clinicopathologic foundations of medicine [4th ed., p. 511]. Philadelphia: Lippincott Williams & Wilkins.)
  • FIGURE 22-11 • Atherosclerotic aneurysm of the abdominal aorta. The aneurysm has been opened longitudinally to reveal a large thrombus in the lumen. The aorta and common iliac arteries display complicated lesions of atherosclerosis. (From Gotlieb A. I. [2005]. Blood vessels. In Rubin E., Gorstein F., Rubin R., et al. [Eds.], Pathology: Clinicopathologic foundations of medicine [4th ed., p. 511]. Philadelphia: Lippincott Williams & Wilkins.)
  • FIGURE 22-13 • The skeletal muscle pumps and their function in promoting blood flow in the deep and superficial calf vessels of the leg.
  • FIGURE 22-12 • Superficial and deep venous channels of the leg. (A) Normal venous structures and flow patterns. (B) Varicosities in the superficial venous system are the result of incompetent valves in the communicating veins. The arrows in both views indicate the direction of blood flow. (Modified from Abramson D. I. [1974]. Vascular disorders of the extremities [2nd ed.]. New York: Harper & Row.)
  • Stasis Dermatitis – inflammatory skin disease
  • PentoxifylinePhosphodiesterase inhibitor which raises intracellular cAMP levels
  • Supplementation with Pyridocine for Hyperhomocysteinemia reduces the concentration of homocysteineInability to inactivate Factor 5 will lead to hypercoagulable state
  • FIGURE 22-15 • Common sites of venous thrombosis. (A) Superficial thrombophlebitis. (B) Most common form of deep thrombophlebitis. (C, D) Deep thrombophlebitis from the calf to iliac veins. (From Haller J. A. Jr. [1967]. Deep thrombophlebitis: Pathophysiology and treatment. Philadelphia: W. B. Saunders.)
  • 23-5 • Two ways in which the arterial pressure can be increased: (A) byshifting the renal output curve in the right-hand direction toward a higher pressure level,and (B) by increasing the intake of salt and water. (From Guyton A. C., Hall J. E. [2006].Textbook of medical physiology [11th ed., p. 218]. Philadelphia: Elsevier Saunders.)
  • The Shy-Drager syndrome usually develops in middl e to late l ife as orthostatic hypotension associated withuncoordinated movements, urinary incontinence, constipation, and other signs of neurologic deficitsreferable to the corticospinal, extrapyramidal, corticobulbar, and cerebellar systems.
  • The Shy-Drager syndrome usually develops in middle to late life as orthostatic hypotension associated withuncoordinated movements, urinary incontinence, constipation, and other signs of neurologic deficitsreferable to the corticospinal, extrapyramidal, corticobulbar, and cerebellar systems.

Vascular Disease Hypertension Disorders of Cardiac Function Vascular Disease Hypertension Disorders of Cardiac Function Presentation Transcript

  • M Sarwar MD
    Miami Dade PA Program
    Vascular DiseaseHypertensionDisorders of Cardiac Function
  • Disorders of Blood Flow in the Systemic Circulation
    Vascular Disease
  • Blood Vessel Structure and Function
    Endothelial Cell
    Vascular Smooth Muscle
    Tunica Intima
    Endothelial cells
    Tunica Media
    Vascular smooth muscle
    Tunica Externa
    Loosely woven collagen
  • Endothelium
    Continuous lining of cells in the vessel
    Plays role in control of platelet adhesion
    Blood clotting
    Modulation of blood flow
    Vascular resistance
    Influence growth of vascular smooth muscle cells -
  • Influences Growth of Smooth Muscle
    Growth Stimulation Factors
    Platelet Derived Growth Factor
    Hematopoietic Colony Stimulating Factor
    Growth inhibiting factors
    Transforming Growth Factor-b
  • Vascular Smooth Muscle Cells
    Predominantly in Tunica Media
    Vasoconstriction or dilation
    Sympathetic fibers release norepinephrine which diffuses into tunica media
    Synthesize collagen, elastin
  • 3 types of Arteries
    Large Elastic Arteries
    Aorta and distal branches
    Medium-sized arteries
    Coronary and renal arteries
    Small arteries and arterioles
    Pass through tissues
  • Triglycerides
  • Lipids in our blood
    Triglycerides - hydrophobic
    Energy metabolism
    Phospholipids – hydrophilic and hydrophobic
    Structural constituents of lipoproteins
    Blood clotting components, myelin, cell membranes
    Cholesterol – hydrophilic and hydrophobic
    Helps to maintain fluidity in cell membranes
    Too much is bad  lead to hypercholesterolemia
    Leading cause of heart attacks, strokes or CV event linked to atherosclerosis – will discuss
  • Lipoproteinencapsulation of cholesterol and triglyceride
    Encapsulated by a stabilizing coat of water soluble phospholipids
  • Lipoproteinencapsulation of cholesterol and triglyceride
    Encapsulated by a stabilizing coat of water soluble phospholipids
    5 types:
    Chylomicrons (SI)
    Very-low-density lipoprotein (VLDL)(liver)IDL
    Intermediate-density lipoprotein (IDL) LDL
    Low density lipoprotein (LDL)(main carrier of cholesterol)
    High density lipoprotein (HDL)(50%)(liver)
  • Too Much LDL  Atherosclerosis
    Monocytes/macrophages can take up LDL
    If there is too much present they can form foam cells in the lumen of the artery
    HDL – facilitates clearance of cholesterol
    ATP – binding cassette transporter A Class1 (ACBA1)
    Defects lead to accelerated atherosclerosis
    Tangier Disease
    Smoking and Metabolic Syndrome associated with decreased levels of HDL
  • Screening of Lipids
    Adults older that 20 years of age
    Have a lipid panel done 1X every 5 years
  • LDL Cholesterol
    < 100 Optimal
    100-129 Near Optimal/
    above optimal
    130-159 Borderline high
    160-189 High
    >=190 Very High
  • Total Cholesterol
    <200 Desirable
    200-239 Borderline High
    >= 240 High
  • HDL Cholesterol
    < 40 Low
    >= 60 High
  • Primary Hypercholesterolemia
    Elevated cholesterol levels independent of other health problems
    Genetic Basis
    IE., Defective apoproteins, lack of receptors, defective receptors
    Secondary Hypercholesterolemia
    Associated with health problems and behaviors
    Lyfestyle – (ex. fast food)
  • Classification of Hyperlipoproteinemias
  • Risk Factors
    Cigarette smoking
    Family hx of premature CHD in 1 Degree relative
    Men >= 45 yrs
    Women >= 55 yrs
    HDL < 40 mg/dL
    Negative Risk Factor
    High HDL >= 60 mg/dL
  • Management
    Reduce Risk Factors:
    Cigarette smoking
    HDL < 40 mg/dL
    Increase Negative Risk Factor
    High HDL >= 60 mg/dL
  • LDL Goals
    0 Risk Factors  160 mg/dL or less
    2 or more RF  130 mg/dL or less
    High RF  100 mg/dL or less
    Very High RF  70 mg/dL or less
  • Management
    Dietary Therapy
    minimum of 3 months of intensive diet therapy be undertaken before drug therapy is considered, unless high risk
    Drug Therapy
    decreasing cholesterol production
    decreasing cholesterol absorption from the intestine
    removing cholesterol from the bloodstream
  • Drugs
    HMG-CoAReductase Inhibitors
    Key enzyme-cholesterol pathway
    Bile Acid-Resin
    Bind to cholesterols in intestines
  • Drugs
    Absorption Inhibitor
    Niacin Congener
    Blocks Synthesis and release of cholesterol
    Nicotinic Acid
    Decrease VLDL synthesis and enhance clearance of triglicerides
  • Atherosclerosis
  • Atherosclerosis
    Hardening of the arteries
    Formation of fibrofatty lesion in the intimal lining of large and medium sized arteries
    Aorta, branches of the arteries, coronary arteries
    Coronary Heart Disease is the leading cause of death in US
  • Risk Factors
    Epidemiology Considerations:
    Men: ≥45 years
    Women: ≥55 years or premature menopause without estrogen replacement therapy
    Family history of premature coronary heart disease (definite myocardial infarction or sudden death before 55 years of age in father or other male first-degree relative, or before 65 years of age in mother or other female first-degree relative)
    Hypertension (≥140/90 mm Hg* or on antihypertensive medication)
    Low HDL cholesterol (<40 mg/dL*)
    Diabetes mellitus
  • Risk Factors Continued
    Current cigarette smoking
    Endothelial dysfunction may be worsened by cigarette smoke
    Elevated CRP levels
    Acute inflammatory phase reactant
    Associated with vascular diseases
  • Atherosclerotic Placques
    Mechanism of Development
  • Development of Atherosclerosis
    (1) endothelial cell injury,
    (2) migration of inflammatory cells,
    (3) smooth muscle cell proliferation and lipid deposition
    (4) gradual development of the atheromatous plaque with a lipid core.
  • Endothelial Cell Injury
  • Migration of Inflammatory Cells
  • Lipid Accumulation and Smooth Muscle Cell Proliferation
  • Plaque Structure
  • Clinical Manifestations
    They narrow the vessels
    This may lead to ischemia (>70% must be compromised in the heart before it becomes symptomatic)
    Sudden vessel obstruction can occur
    Aneurysm Formation (weakening of wall)
  • MaxonC4D
  • Ischemia
    Reduction of blood flow
    Oxygen demands not being met
    Oxygen demands not met until the point of cell death
    Ischemia that leads to necrosis
  • Vasculitis - Vasculitides
    Vascular disorders that cause inflammatory injury and necrosis of the blood vessel wall
    Involvement of endothelial cells and smooth muscles of vessel wall
  • Vasculitis – VasculitidesClinical Manifestations
  • Vasculitis - Etiology
    Direct injury
    Infection agents
    Immune process (ANCA)
    Secondary (due to other processes)
    Cold, Mechanical, toxins
  • Groups of Vasculitides Table 22-4
    Small Vessel Vasculitis
    Microscopic Polyangitis
    Wegener Granulamatosis
    Medium Sized Vessel Vasculitis
    Kawasaki Disease
    Large Vessel Vasculitis
    Giant cell (Temporal) Arteritis
  • Small Vessel Vasculitiscapillaries, venules, arterioles
    Microscopic Polyangitis
    Few or no immune deposits, medium and small blood vessels
    Necrotizing glomerulonephritis
    Pulmonary Involvement
    Wegener Granulamatosis
    Granulomatous inflammation involving repsiratory
    Necrotizing glomerulonephritis
    Includes arteries
  • Medium Sized vessel vasculitisPolyarteritisNodosa
    Necrotizing inflammation, lacks vasculitis in arteries
    Secondary to underlying disease or environmental agent, numerous nodules
    Reddish blue, mottled areas of discoloration skin on extremity  livedoreticularis, purpura, urticaria and ulcers
    Labs: Elevated ESR, leukocytosis, anemia
    Dx: Biopsy is confirmatory
    Tx: High dose corticosteroids and immunosuppressive agents (18-24 mos. then tapered)
    5 year survival > 50%
  • Medium Sized vessel vasculitis
    Kawasaki Disease
    Large, medium and small arteries (coronaries)
    Associated with mucocutaneous lymph node syndrome (small children)
    High persistent fever usually greater than 102 degrees
    Does not go away with Acetaminophen
    Tx: IV Gamma Globulin,
    High dose aspirin
  • Medium Sized vessel vasculitis
    ThromboangitisObliterans (Buerger disease)
    Segmental, thrombosing, acute and chronic
    Medium and small arteries, tibial and radial arteries
    Veins and nerves of extremities,
    Peripheral Vascular Disease
    Predominantly Men 25-40 yrs, heavy smokers
  • ThromboangitisObliterans(Buerger disease)
    STOP Smoking
    Increasing vasodilatation to those tissues
    Sympathectomy may be done
    Decreases vasospasms
  • Raynaud Disease and Phenomenon
    Raynaud Disease
    Occurs without demonstratable cause
    Exposure to cold or Emotions (common in women)
    Raynaud Phenomenon
    Associated with other disease states
    Precedes Scleroderma (collagen disease)
  • Raynaud Disease and Phenomenon
    Ischemia due to vasospasm
    After ischemia, period of hyperemia with redness
    Throbbing and parasthesias
    Bases on history of vasospastic attacks
    Abstinence from smoking and cold
    Vasodilator drugs may be indicated, CCB, Prazosin
  • Large Vessel VasculitisGiant cell (Temporal) Arteritis
    Granulomatous inflammation of aorta, major branches (focal inflammatory)
    Predilection for extra cranial vessels
    > 50 yrs, associated with polymyalgiarheumatica 2:1 female to male ratio
    Sudden headache, tenderness over artery, blurred vision or diplopia
    Dx Elevated ESR, CRP, Biopsy
    Tx High dose corticosteroids
    otherwise may risk 80% blindness
  • Large Vessel Vasculitis
    Granulomatous inflammation of aorta and branches
    < 50 yrs of age, in younger people
  • Arterial Diseases of the ExtremityPeripheral Vascular Diseases
    Acute Arterial Occlusion
    Sudden event that interrupts flow
    Embolus – freely moving particle, heart is source in most cases, prosthetic heart valves
    Fat emboli
    Air Emboli
    Thrombus - Blood clot that forms on vessel wall and grows until it occludes the vessel
    Symptoms depend on artery affected
  • Arterial Diseases of the ExtremityPeripheral Vascular Diseases
    Acute Arterial Occlusion
    7 P’s
    Pistol shot (acute)
    Polar (cold)
  • Arterial Diseases of the ExtremityPeripheral Vascular Diseases
    Acute Arterial Occlusion
    Diagnosis and Treatment
    Dx: Signs of impaired blood flow
    Visual Assesment
    Tx aimed at restoring blood flow
    Embolectomy (surgical removal)
    Anticoagulation (heparin, prevents growth)
  • Arterial Diseases of the ExtremityPeripheral Vascular Diseases
    Atherosclerotic Occlusive Disease
    Peripheral Artery Disease (lower extremities)
    Arteriosclerosis obliterans
    Superficial femoral and popliteal commonly affected
    Men in 60’s and 70’s
    Risk Factors
    Cigarette smoking and Diabetes Mellitus
    50 – 70% narrowing before symptoms arise
    Intermittent claudication or pain while walkingAffected limb is cool, pulses diminished
    Worse while laying, improved while standing
  • Arterial Diseases of the ExtremityPeripheral Vascular Diseases
    Atherosclerotic Occlusive Disease
    Palpation of pulses
    BP Rations, ankle to arm, less than 0.9 indicate occlusion
    Doppler ultrasound may be used to detect pulses if palpation does not work
    MIR, Spiral CT arteriography, invasive contrast angiography
  • Arterial Diseases of the ExtremityPeripheral Vascular Diseases
    Atherosclerotic Occlusive Disease
    Decrease Risk Factors
    Smoking, HTN, DM
    Reduction of Symptoms
    Antiplatelet agents (aspirin or clopidogrel)
    Percutaneoustransluminal angioplasty
    Stent placement
    Surgery (bypass procedures)
  • Aneurysms and Dissection
    An aneurysm is an abnormal localized dilation of a blood vessel
    True Aneurysm
    Bounded by a complete vessel wall
    False Aneurysm (pseudoaneurysm)
    Bounded by outer layers of vessel wall
  • Types of Aneurysms
    Entire circumference involved
    Extends over part of the cercumference (saclike)
    False aneurysm, resulting from tear in the intima
    Blood filled cavity
  • Etiology
    Congenital defects
  • Aortic Aneurysms
    Ascending Aorta
    Aortic arch
    Descending Aorta
    2 Most Common Causes
    9% of people older than 65, ~15,000 deaths a year in US
  • Aortic AneurysmsManifestations
    Size and location
    May present with substernal, back or neck pain
    Dyspnea, stridor or brassy cough (pressure on trachea)
    Hoarseness (recurrent laryngeal nerve)
    Difficulty swallowing
  • Abdominal Aortic Aneurysm
    >90% located below renal artery
    Pulsating mass may be notices
    > 4 cm to become palpable (normal abdominal aorta is 2 cm)
    May be calcified
    Complication  Rupture
  • Diagnosis and Treatment
    CT scans
    Surgical Repair (synthetic graft of woven Dacron)
  • Aortic Dissection
    Caused by conditions that weaken or cause degenerative changes in the elastic and smooth muscle layers of aorta
    40-60 year old age group
    Risk Factors
    Degeneration of the medial layer of the vessel wall
    Connective tissue diseases (ex. Marfans Syndrome)
    Congenital defects
  • Aortic Dissection Classification
    Type I – Ascending to descending
    Type II – Ascending stops before great vessels
    Type III – distal to left subclavian
    Sanford – more mainstream
    Type A – involves ascending
    Type B – spares ascending aorta
  • Aortic Dissection
    Abrupt Presence of excruciating pain
    Described as tearing or ripping
    • Type A – involves ascending
    Anterior chest wall pain
    • Type B – spares ascending aorta
    Back pain
    As dissection spreads, BP’s may diminish in affected limbs, hemiplegia or paralysis
    Heart failure with involvement of Aortic Valve
  • Diagnosis
    Physical Exam
    Aortic Angiography
    Trans-esophageal echocardiography
    CT scans
    MRI studies
  • Treatment
    Decrease force of systole from heart
    IV sodium nitroprusside and B-adrenergic blocker
    Resection of the involved segment of the aorta, replacement with a prosthetic graft
  • Disorders of Venous Circulation
    Varicose Veins
    Dilated, tortuous Veins of lower extremities
    Primary – originate from superficial saphenous vein
    Secondary – impaired flow in deep venous channels (DVT, congenital, pregnancy, tumor)
  • Mechanisms
    Prolonged Standing - gravity
    Increased intra-abdominal pressure (pregnancy)
    Defective Venous valves
    Hormonal effect (venous dilation)
    Heavy Lifting
    Obesity reduces support provided by the superficial fascia
  • Manifestation
    Unsightly appearance
    Aching in the lower extremities
    Edema (subsides at night)
  • Diagnosis and Treatment
    Physical Inspection
    Trendelenburg test
    Test Filling for superficial veins
    Emptying is for Deep Veins
    Elastic Support stocking or leggings compress to prevent distention
    Sclerotherapy (produces fibrosis of the vessel lumen, for small residual vericosities)
    Surgical – removal of varicosities, deep veins must be patent
  • Chronic Venous Insufficiency
    Tissue congestion, edema
    Impairment of tissue nutrition
    Necrosis of subcutaneous fat deposits
    Brown pigmentation of skin (hemosederin)
    Secondary Lymphatic insufficiency, progressive sclerosis of lymph channels due to increased interstitial fluid
    Stasis Dermatitis and Venous ulcers
  • Treatment
    Venous ulcers  compression therapy with dressings
    Medications (aspirin and pentoxifyline)
    Skin grafting may be required
    Growth factors (topical or injection)
  • Venous ThrombosisThrombophlebitis
    Presence of thrombus in a vein
    Accompanying inflammatory response in vessel wall
    Superficial or deep veins
    Can lead to Pulmonary Embolism
    (Sitting for long periods of time, ex airplane)
  • Virchow's Triad
  • DVT’s
    Inherited Risk factors
    Factor V Leiden and prothrombin gene mutations
    Postpartum state (increased fibrinogen, prothrombin)
    Oral Contraceptives and HRT (increases coagulability, increases in females who smoke)
    Antiphospholipid Syndrome
  • DVT - Manifestations
    Mostly Asymptomatic (as much as 50%)
    When Symptomatic, similar to inflammatory process
    Pain, swelling, deep muscle tenderness
    Fever, general malaise, elevated WBC and ESR
    When present in calf veins
    Active dorsiflexion creates pain (Homans sign)
  • DVT - Diagnosis
    Ascending Venography
    Plasma D-dimer assessment
  • DVT- Treatment
    Post partum, early ambulation
    Anti-embolism stockings
    Pneumatic Compression device
    These devices help enhance venous emptying
    Elevation of leg 15 – 20 degrees helps prevent stasis
    Gradual ambulation with elastic support
  • DVT - Treatment
    Anticoagulation Therapy (heparin and warfarin)
    Treats and prevents
    Initiated by IV heparin
    Oral prophylaxis
    SubQ injections
    Thrombolytics may be used to dissolve
    Surgical Removal
    Intracaval filters may be done in high risk patients
  • Hypertension
  • Hemodynamics
    most variable, but best regulated functions of the body
    keep blood flow constant to vital organs
    BP Elevation –> primary contributor to premature death and disability
    heart, blood vessels, and kidneys
  • Approximately 70% of the blood that leaves the left ventricle is ejected during the first one third of systole (EF)
    Rapid rise in the pressure contour. The end of systole is marked by a brief downward decrease in BP
  • Pulse Pressure
    Ejection Fraction
    Systolic Pressure
    Diastolic Pressure
    Mean Arterial Pressure
    Determined by?
  • Short-Term Regulation
  • Neural Mechanism
    ANS – Reticular formation of the medulla and lower third of the pons
    Parasympathetic impulses via vagus nerve to heart
    Sympathetic Stimulation increases HR and Contractility
    Blood Vessels  increase in TPR
  • Neural Mechanism
    Intrinsic Reflexes
    Baroreceptors (pressure sensitive receptors)
    Carotid, Aortic
    Chemoreceptors (located in baroreceptors)
    Oxygen, CO2, Hydrogen Ions
    Extrinsic Reflexes
    Control centers found outside of circulation
  • Humoral Mechanisms.
    Renin-Angiotensin System
    Juxtaglomerular Apparatus
    Macula Densa Senses change in osmolarity or Na levels
    Renin is Released
    Vasopressin Aka (ADH)
    Released from the Pituitary Gland
    Hypothalamus Is the control center
  • Why do we get Blood Pressure
    Properties of Arterial System
    Systolic and Diastolic Components
    Blood Volume
    Elastic Properties
    Cardiac Output
    Peripheral Vascular Resistance
  • Systolic BP
    Amount of blood ejected
    Large amount of ejection moves into arteries
    Pressure increases with aging and vessels loose their elasticity
  • Diastolic BP
    Reflects closure of aortic valve
    Elasticity in vessels help maintain forward flow
  • R-A System
    Renin (hormone) release by juxtaglomerular cells in kidney
    Increase in sympathetic nervous system activity
    Decrease in MAP, Blood Pressure
    Angiotensinogen gets converted in the presence of Renin to Angiotensin I
    Angiotensin I  Angiotensin II
    Via ACE in endothelial cells in the pulmonary system
  • Vascular Volume &
    Arterial Blood Pressure
    Goes up
  • Angiotensin II
    Potent Vasoconstricter
    Increase Na reabsorption in proximal tubule of nephron (kidneys)
    Stimulate the release of AldosteroNe
    Salt and Water reabsorption in the Collecting Ducts in the Kidney
    Vassopressin (ADH) released from posterior pituitary in response to decreas in BP and increase in osmolarity of plasma
    Vasoconstrictor of splanchnic system (abdomen)
  • Long-Term Regulation
    Daily, weekly and monthly regulation
    Largely vested by the kidneys in regulation of the ECF
    Many Blood Pressure medications work here
  • Increases in Fluid Volume  BP
    Cardiac output
    Blood flow to various tissues according to their needs
  • Increase renal retention of fluids
    Increase Na and H20 input
  • HTN - Hypertension
    Essential Hypertension
    chronic elevation in blood pressure that occurs without evidence of other disease
    essential hypertension is thought to include constitutional and environmental factors
    left ventricular hypertrophy and heart failure, and on the vessels of the arterial system, leading to atherosclerosis, kidney disease, retinopathy, and stroke
  • Classification of BP
    Systolic Diastolic
    Normal < 120 < 80 F/U 2 yrs
    Pre HTN 120-139 80-89 F/U 1 yrs
    Stage 1 HTN 140-159 90-99 F/U 2 mo
    Stage 2 HTN > 160 > 100
  • Risk Factors
    Family History
    Age-Related Changes in Blood Pressure.
    Race (more severe in africanamericans)
    Insulin Resistance and Metabolic Abnormalities
    Increases CAD 4X
  • Risk Factors
    Lifestyle Risk Factors
    High Salt Intake.
    Obesity. (Syndrome X)
    (angiotensinogen/leptin/increase aldosterone)
    Excess Alcohol Consumption
    Dietary Intake of Potassium, Calcium, and Magnesium.
  • Target-Organ Damage
    Stroke, dementia and cognitive impairment
    Retinal Complications
    Retinopathy, Vascular Hemorrhages
  • Treatment
    JNC 7 report contains a treatment algorithm
    Next Slide, review
    Secondary hypertension
    Lifestyle Modification.
  • Treatment
    β-Adrenergics blockers
    ACE Inhibitors (cough)
    Inhibit bradykinin
    Calcium Channel Receptor Blocking Drug
    α1 receptor antagonist
    α2 receptor agonist (clonidine)
  • Treatment Strategies
    A regimen that helps with adherence
    Side effects
    Number of doses to take
  • Circadian VariationDippers versus non dippers
    Dippers exhibit normal variations
    Non-dippers may have an underlying disease
    Malignant Hypertension
    Orthostatic Hypotension
    Congestive Heart Failure
  • Systolic Hypertension
    Leads to hypertrophy of the heart
    Heart requires increase in oxygen supply
    Greater risk of ischemia
  • Secondary Hypertension
    Many causes can be cured by medicine or surgery
    Cocaine, amphetamine
    Kidney disease, pheochromocytoma, coarctation of the aorta
    Oral Contraceptive Drugs
    Increase R-A pathway
  • Renal Hypertension
    Most common cause of secondary hypertension in older individuals (> 50 yrs)
    Atherosclerosis of renal artery
    < 30 yrs, female, fibromuscular dysplasia
    Tx: Control BP and maintain renal function
  • Disorders of Adrenocortical Hormones
    Cushings Disease (increase in cortisol)
    Increase in ACTH can increase BP
    Salt and Water resabsorption in kidney
    Aldosterone levels increased
    May need K Sparing Diueretics
    Spironolactone (Aldosteroneantaganist)
    Blocks Principal Cells in Collecting Ducts
  • Pheochromocytoma
    Tumor of Chromaffin tissue (adrenal medulla)
    Can arise in sympathetic ganglia
    Catecholamine's, Epinephrine and Norepinephrine
    Headache, palpitations, excessive sweating
    50%  paroxysmal
    50%  Sustained
  • Diagnostic Tests
    Urinary Catecholamines and their metabolites
    Plasma Catecholamines
    Tumor must be located and removed
    If unresectable Tx with drug to block
  • Coarctation of the Aorta
    Narrowing just distal to the sublcavian
    Blood flow to lower parts of body reduced
    Including kidney
    Activates R-A Pathway due to decrease BP
    Pressure difference > 20 mmHg when comparing arms versus legs indicates Coarctation
    Tx: Surgical Repair or Balloon Angioplasty
  • Oral Contraceptive Drugs
    Largely unknown, research indicates that is probably related to the R-A pathway which leads to an increase in Na retention
  • Malignant Hypertension
    Sudden marked elevation of Blood Pressure
    Diastolic Values greater than 120 mmHg
    Intense spasms of cerebral arteries
    Hypertensive Encephalopathy
    Papilledema (on opthalmascopic examination)
    Injury to arteriole walls if untreated
    Tx : Emergency! Partial reduction of BP
  • High Blood Pressure in Pregnancy
    After 1st 20 wks, proteinuria – HELLP Syndrome
    Gestational Hypertension.
    BP increased, without proteinuria, returns to normal 12 week postpartum
    Chronic Hypertension.
    BP elevated > 140 systolic, persists after pregnancy
    Preeclampsia Superimposed on Chronic Hypertension.
    BP > 140 systolic, with proteinuria
  • Diagnosis and Treatment
    Early Prenatal care is essential
    Preeclampsia, delivery of fetus is curative
    Depends on timing
    Survival of fetus mainly depends on the level of lung maturity
    Medication must be carefully chosen, may be harmful to the fetus
  • High Blood Pressure in Children and Adolescents
    Lifestyle factors have been increasing this
    Obesity and decreased exercise
    Review 23-4
    Mostly due to secondary causes
    Coarctation of aorta, kidney abnormalities
    Endocrine, Pheochromocytomaor Cortisol, rare
    Nephrotoxicity of Cyclosporine
  • Diagnosis and Treatment
    BP should be checked once a year
    Preferably non-pharmacologic treatment
    Lifestyle modification
    Pharmacologic treatment
  • High Blood Pressure in the Elderly
    Rate of HTN increases;
    > 60 yrs ~50%, > 70 yrs ~ 75%
    Stiffening of arterial vessels, decreased baroreceptor sensitivity, increased PVR
    Elastin fibers in walls degrade
    Pulse pressure widens
    Diagnosis and Treatment
    Blood Pressure
    Follow JNC-7 – same as general population
    Pathophysiology and Causative Factors
    500-700 ml of blood shifted while standing
    Usually transient, lasting 2-3 cardiac cycles
    Baroreceptors sense change  ANS, ADH
    Medications and disease processes in elderly
    Decreased Systolic, decreased sensitivity to pressure changes (baroreceptors)
    Reduced Blood Volume.
    Excessive use of diuretics, vomiting, diarrhea
    Bed Rest and Impaired Mobility.
    Reduction in plasma volume, failure of peripheral vasoconstriction
    Drug-Induced Hypotension
    Antihypertensive Drugs
    Psychotropic Drugs
    Change drug or reduce dosage
    Disorders of the Autonomic Nervous System.
    3 types of primary ANS dysfunction
    Pure Autonomic Failure
    ParkinsonsDz with Autonomic Failure
    Multiple System Atrophy
    Shy-Drager Syndrome – middle to late life
    Diagnosis and Treatment
    Check BP Standing and while Supine
    No change in HR (baroreceptor dysfunction)
    Tachycardia (hypovolemia)
    PharmocologicTx when all other fails
    Drugs that act on resistance vessels
  • JNC – 8
    Coming to Journals soon in your area!!
    JNC – 8
    Available March 2010