Vascular Disease Hypertension Disorders of Cardiac Function

M Sarwar MDMiami Dade PA ProgramVascular DiseaseHypertensionDisorders of Cardiac Function

Disorders of Blood Flow in the Systemic CirculationVascular Disease

Blood Vessel Structure and FunctionEndothelial CellVascular Smooth Muscle

Tunica IntimaEndothelial cellsTunica MediaVascular smooth muscleTunica Externa Loosely woven collagen tissue

EndotheliumContinuous lining of cells in the vesselPlays role in control of platelet adhesionBlood clotting

Modulation of blood flowVascular resistanceInfluence growth of vascular smooth muscle cells -

Influences Growth of Smooth MuscleGrowth Stimulation FactorsPlatelet Derived Growth FactorHematopoietic Colony Stimulating FactorGrowth inhibiting factorsHeparinTransforming Growth Factor-b

Vascular Smooth Muscle CellsPredominantly in Tunica MediaVasoconstriction or dilation

Sympathetic fibers release norepinephrine which diffuses into tunica media

Synthesize collagen, elastin

3 types of ArteriesLarge Elastic ArteriesAorta and distal branches

Medium-sized arteriesCoronary and renal arteries

Small arteries and arteriolesPass through tissues

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TriglyceridesCholesterolPhospholipids

Lipids

Lipids in our bloodTriglycerides - hydrophobicEnergy metabolism

Phospholipids hydrophilic and hydrophobicStructural constituents of lipoproteinsBlood clotting components, myelin, cell membranes

Cholesterol hydrophilic and hydrophobicHelps to maintain fluidity in cell membranesToo much is bad lead to hypercholesterolemiaLeading cause of heart attacks, strokes or CV event linked to atherosclerosis will discuss

Lipoproteinencapsulation of cholesterol and triglycerideEncapsulated by a stabilizing coat of water soluble phospholipids

Lipoproteinencapsulation of cholesterol and triglycerideEncapsulated by a stabilizing coat of water soluble phospholipids

5 types:Chylomicrons (SI)Very-low-density lipoprotein (VLDL)(liver)IDLIntermediate-density lipoprotein (IDL) LDLLow density lipoprotein (LDL)(main carrier of cholesterol)High density lipoprotein (HDL)(50%)(liver)

Too Much LDL AtherosclerosisMonocytes/macrophages can take up LDLIf there is too much present they can form foam cells in the lumen of the artery

HDL facilitates clearance of cholesterolATP binding cassette transporter A Class1 (ACBA1)Defects lead to accelerated atherosclerosisTangier DiseaseSmoking and Metabolic Syndrome associated with decreased levels of HDL

Screening of LipidsAdults older that 20 years of ageHave a lipid panel done 1X every 5 years

LDL Cholesterol

< 100Optimal100-129Near Optimal/ above optimal130-159Borderline high160-189High>=190Very High

Total Cholesterol

= 240High

HDL Cholesterol

< 40Low>= 60High

Primary HypercholesterolemiaElevated cholesterol levels independent of other health problemsGenetic BasisIE., Defective apoproteins, lack of receptors, defective receptors

Secondary HypercholesterolemiaAssociated with health problems and behaviorsLyfestyle (ex. fast food)

Classification of HyperlipoproteinemiasTYPEFAMILIAR NAMELIPOPROTEIN ABNORMALITYUNDERLYING GENETIC DEFECTS1Exogenous dietary hypertriglyceridemiaElevated chylomicrons and triglyceridesMutation in lipoprotein lipase gene2aFamilial hypercholesterolemiaElevated LDL cholesterolMutation in LDL receptor gene or in apoprotein B gene2bCombined hyperlipidemiaElevated LDL, VLDL, and triglyceridesMutation in LDL receptor gene or apoprotein B gene

TYPEFAMILIAR NAMELIPOPROTEIN ABNORMALITYUNDERLYING GENETIC DEFECTS3Remnant hyperlipidemiaIncreased remnants (chylomicrons), IDL triglycerides, and cholesterolMutation in apolipoprotein E gene4Endogenous hypertriglyceridemiaElevated VLDL and triglyceridesUnknown5Mixed hypertriglyceridemiaElevated VLDL, chylomicrons, and cholesterol; triglycerides greatly elevatedMutation in apolipoprotein C-II gene

Xanthomas in skin or tendonsArcus lipoides21

Risk FactorsCigarette smokingHTNFamily hx of premature CHD in 1 Degree relativeMen >= 45 yrsWomen >= 55 yrsHDL < 40 mg/dLNegative Risk FactorHigh HDL >= 60 mg/dLHDL

ManagementReduce Risk Factors:Cigarette smokingHTNHDL < 40 mg/dLIncrease Negative Risk FactorHigh HDL >= 60 mg/dLHDL

LDL Goals0 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

ManagementDietary Therapyminimum of 3 months of intensive diet therapy be undertaken before drug therapy is considered, unless high risk

Drug Therapydecreasing cholesterol productiondecreasing cholesterol absorption from the intestineremoving cholesterol from the bloodstream

DrugsHMG-CoA Reductase InhibitorsKey enzyme-cholesterol pathwayBile Acid-ResinBind to cholesterols in intestinesAtorvastatinRosuvastatinSimvastatinCholestyramineColestipolColesevelam

DrugsAbsorption InhibitorNiacin CongenerBlocks Synthesis and release of cholesterolExetimibeNicotinic Acid

FibratesDecrease VLDL synthesis and enhance clearance of trigliceridesFenofibrateGemfibrozil

Atherosclerosis

AtherosclerosisHardening of the arteries

Formation of fibrofatty lesion in the intimal lining of large and medium sized arteriesAorta, branches of the arteries, coronary arteriesCoronary Heart Disease is the leading cause of death in US

Risk FactorsEpidemiology Considerations:AgeMen: 45 yearsWomen: 55 years or premature menopause without estrogen replacement therapyFamily 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 (70% must be compromised in the heart before it becomes symptomatic)Sudden vessel obstruction can occurAneurysm Formation (weakening of wall)

MaxonC4D

AstraZeneca

http://www.youtube.com/watch?v=oZJlZywgQL8http://www.youtube.com/watch?v=fLonh7ZesKs&feature=related

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IschemiaReduction of blood flowOxygen demands not being met

InfarctionOxygen demands not met until the point of cell deathIschemia 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

FeverMyalgiaArthralgiamalaise

Vasculitis - EtiologyPrimaryDirect injuryInfection agentsImmune process (ANCA)

Secondary (due to other processes)SLECold, Mechanical, toxins

Anti Neutrophil Cytoplasmic Antibodies46

Groups of Vasculitides Table 22-4Small Vessel VasculitisMicroscopic PolyangitisWegener GranulamatosisMedium Sized Vessel VasculitisPolyarteritis NodosaKawasaki DiseaseThromboangitis ObliteransLarge Vessel VasculitisGiant cell (Temporal) ArteritisTakayasu Arteritis

Small Vessel Vasculitiscapillaries, venules, arteriolesMicroscopic PolyangitisFew or no immune deposits, medium and small blood vesselsNecrotizing glomerulonephritisPulmonary InvolvementWegener GranulamatosisGranulomatous inflammation involving repsiratoryNecrotizing glomerulonephritis Includes arteries

Medium Sized vessel vasculitisPolyarteritis NodosaNecrotizing inflammation, lacks vasculitis in arteriesSecondary to underlying disease or environmental agent, numerous nodulesReddish blue, mottled areas of discoloration skin on extremity livedo reticularis, purpura, urticaria and ulcersLabs: Elevated ESR, leukocytosis, anemiaDx: Biopsy is confirmatoryTx: High dose corticosteroids and immunosuppressive agents (18-24 mos. then tapered)5 year survival > 50%

Medium Sized vessel vasculitisKawasaki DiseaseLarge, medium and small arteries (coronaries)Associated with mucocutaneous lymph node syndrome (small children)High persistent fever usually greater than 102 degreesDoes not go away with AcetaminophenTx: IV Gamma Globulin, High dose aspirin

Medium Sized vessel vasculitisThromboangitis Obliterans (Buerger disease)Segmental, thrombosing, acute and chronicMedium and small arteries, tibial and radial arteriesVeins and nerves of extremities,

Peripheral Vascular DiseasePredominantly Men 25-40 yrs, heavy smokers

Thromboangitis Obliterans (Buerger disease)TreatmentSTOP SmokingIncreasing vasodilatation to those tissuesSympathectomy may be doneDecreases vasospasms

Raynaud Disease and PhenomenonRaynaud DiseaseOccurs without demonstratable causeExposure to cold or Emotions (common in women)

Raynaud PhenomenonAssociated with other disease statesPrecedes Scleroderma (collagen disease)

Raynaud Disease and PhenomenonManifestationsIschemia due to vasospasmAfter ischemia, period of hyperemia with rednessThrobbing and parasthesiasDiagnosisBases on history of vasospastic attacksTreatmentAbstinence from smoking and coldVasodilator drugs may be indicated, CCB, PrazosinSympathectomy

CCB Calcium Channel Blocker, Prazosin (alpha blocker)56

Large Vessel VasculitisGiant cell (Temporal) ArteritisGranulomatous inflammation of aorta, major branches (focal inflammatory)Predilection for extra cranial vessels> 50 yrs, associated with polymyalgia rheumatica 2:1 female to male ratioSudden headache, tenderness over artery, blurred vision or diplopiaDx Elevated ESR, CRP, BiopsyTx High dose corticosteroidsotherwise may risk 80% blindness

Cause unknown, autoimmune suggestion, 10% Risk of aortic anuerysm58

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.)59

Large Vessel VasculitisTakayasu Arteritis

Granulomatous inflammation of aorta and branches< 50 yrs of age, in younger people

Arterial Diseases of the ExtremityPeripheral Vascular DiseasesAcute Arterial OcclusionSudden event that interrupts flowEmbolus freely moving particle, heart is source in most cases, prosthetic heart valvesFat emboliAir EmboliThrombus - Blood clot that forms on vessel wall and grows until it occludes the vesselSymptoms depend on artery affected

Arterial Diseases of the ExtremityPeripheral Vascular DiseasesAcute Arterial Occlusion7 PsPistol shot (acute)PallorPolar (cold)PulselessnessPainParesthesiaParalysis

Arterial Diseases of the ExtremityPeripheral Vascular DiseasesAcute Arterial Occlusion

Diagnosis and TreatmentDx: Signs of impaired blood flowVisual Assesment

Tx aimed at restoring blood flowEmbolectomy (surgical removal)Anticoagulation (heparin, prevents growth)

Arterial Diseases of the ExtremityPeripheral Vascular DiseasesAtherosclerotic Occlusive DiseasePeripheral Artery Disease (lower extremities)Arteriosclerosis obliteransSuperficial femoral and popliteal commonly affectedMen in 60s and 70sRisk FactorsCigarette smoking and Diabetes Mellitus50 70% narrowing before symptoms ariseIntermittent claudication or pain while walkingAffected limb is cool, pulses diminishedWorse while laying, improved while standing

Arterial Diseases of the ExtremityPeripheral Vascular DiseasesAtherosclerotic Occlusive DiseaseDiagnosisInspectionPalpation of pulsesBP Rations, ankle to arm, less than 0.9 indicate occlusionDoppler ultrasound may be used to detect pulses if palpation does not workMIR, Spiral CT arteriography, invasive contrast angiography

Arterial Diseases of the ExtremityPeripheral Vascular DiseasesAtherosclerotic Occlusive DiseaseTreatmentDecrease Risk FactorsSmoking, HTN, DMReduction of SymptomsAntiplatelet agents (aspirin or clopidogrel)Percutaneous transluminal angioplastyStent placementSurgery (bypass procedures)

Aneurysms and DissectionAn aneurysm is an abnormal localized dilation of a blood vessel

True AneurysmBounded by a complete vessel wall

False Aneurysm (pseudoaneurysm)Bounded by outer layers of vessel wall

Types of AneurysmsBerryFusiformEntire circumference involvedSaccularExtends over part of the cercumference (saclike)DisectingFalse aneurysm, resulting from tear in the intimaBlood filled cavity

Three forms of aneurysms: (A) berry aneurysm in the circle of Willis, (B) aortic dissection, and (C) fusiform-type aneurysm of the abdominal aorta.70

EtiologyCongenital defectsTraumaInfectionsatherosclerosis

Aortic AneurysmsAscending AortaAortic archDescending Aorta

2 Most Common CausesAtherosclerosisHypertension9% of people older than 65, ~15,000 deaths a year in US

Aortic AneurysmsManifestationsSize and locationMay present with substernal, back or neck painDyspnea, stridor or brassy cough (pressure on trachea)Hoarseness (recurrent laryngeal nerve)Difficulty swallowing

Abdominal Aortic Aneurysm>90% located below renal arteryPulsating mass may be notices> 4 cm to become palpable (normal abdominal aorta is 2 cm)May be calcifiedComplication Rupture

Diagnosis and TreatmentUltrasonographyEchocardiographyCT scansMRI

Surgical Repair (synthetic graft of woven Dacron)

Aortic DissectionCaused by conditions that weaken or cause degenerative changes in the elastic and smooth muscle layers of aorta40-60 year old age groupRisk FactorsHTNDegeneration of the medial layer of the vessel wallConnective tissue diseases (ex. Marfans Syndrome)PregnancyCongenital defects

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.)

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Aortic Dissection ClassificationDeBakey Type I Ascending to descendingType II Ascending stops before great vesselsType III distal to left subclavianSanford more mainstreamType A involves ascendingType B spares ascending 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.)

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Aortic DissectionAbrupt Presence of excruciating painDescribed as tearing or rippingType A involves ascendingAnterior chest wall painType B spares ascending aortaBack pain

As dissection spreads, BPs may diminish in affected limbs, hemiplegia or paralysisHeart failure with involvement of Aortic Valve

DiagnosisHistoryPhysical ExamAortic AngiographyTrans-esophageal echocardiographyCT scansMRI studies

TreatmentMedicalHypertensionDecrease force of systole from heartIV sodium nitroprusside and B-adrenergic blocker

SurgicalResection of the involved segment of the aorta, replacement with a prosthetic graft

Disorders of Venous CirculationVaricose VeinsDilated, tortuous Veins of lower extremities

Primary originate from superficial saphenous veinSecondary impaired flow in deep venous channels (DVT, congenital, pregnancy, tumor)

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FIGURE 22-13 The skeletal muscle pumps and their function in promoting blood flow in the deep and superficial calf vessels of the leg.

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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.)84

MechanismsProlonged Standing - gravityIncreased intra-abdominal pressure (pregnancy)Defective Venous valvesHormonal effect (venous dilation)Heavy LiftingObesity reduces support provided by the superficial fascia

ManifestationUnsightly appearanceAching in the lower extremitiesEdema (subsides at night)

Diagnosis and TreatmentPhysical InspectionTrendelenburg testTest Filling for superficial veinsEmptying is for Deep Veins

Elastic Support stocking or leggings compress to prevent distentionSclerotherapy (produces fibrosis of the vessel lumen, for small residual vericosities)Surgical removal of varicosities, deep veins must be patent

Chronic Venous InsufficiencyTissue congestion, edemaImpairment of tissue nutrition

Necrosis of subcutaneous fat depositsBrown pigmentation of skin (hemosederin)Secondary Lymphatic insufficiency, progressive sclerosis of lymph channels due to increased interstitial fluidStasis Dermatitis and Venous ulcers

Stasis Dermatitis inflammatory skin disease88

TreatmentVenous ulcers compression therapy with dressingsMedications (aspirin and pentoxifyline)Skin grafting may be requiredGrowth factors (topical or injection)

PentoxifylinePhosphodiesterase inhibitor which raises intracellular cAMP levels90

Venous ThrombosisThrombophlebitisPresence of thrombus in a veinAccompanying inflammatory response in vessel wallSuperficial or deep veinsCan lead to Pulmonary Embolism(Sitting for long periods of time, ex airplane)

Virchow's Triad

DVTsInherited Risk factorsFactor V Leiden and prothrombin gene mutationsPostpartum state (increased fibrinogen, prothrombin)Oral Contraceptives and HRT (increases coagulability, increases in females who smoke)Antiphospholipid SyndromeHyperhomocysteinemia

Supplementation with Pyridocine for Hyperhomocysteinemia reduces the concentration of homocysteine

Inability to inactivate Factor 5 will lead to hypercoagulable state93

DVT - ManifestationsMostly Asymptomatic (as much as 50%)

When Symptomatic, similar to inflammatory processPain, swelling, deep muscle tendernessFever, general malaise, elevated WBC and ESRWhen present in calf veinsActive dorsiflexion creates pain (Homans sign)

DVT - DiagnosisAscending VenographyUltrasonagraphyPlasma D-dimer assessment

DVT- TreatmentPreventionPost partum, early ambulationAnti-embolism stockingsPneumatic Compression deviceThese devices help enhance venous emptyingElevation of leg 15 20 degrees helps prevent stasisGradual ambulation with elastic support

DVT - TreatmentAnticoagulation Therapy (heparin and warfarin)Treats and preventsInitiated by IV heparinOral prophylaxisSubQ injectionsThrombolytics may be used to dissolveSurgical Removal Intracaval filters may be done in high risk patients

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.)

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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 disabilityheart, 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 PressureEjection Fraction

Systolic PressureDiastolic Pressure

Mean Arterial PressureDetermined by?MAP=CO*PVR

Short-Term Regulation

Neural MechanismANS Reticular formation of the medulla and lower third of the pons

Parasympathetic impulses via vagus nerve to heartSympathetic Stimulation increases HR and ContractilityBlood Vessels increase in TPR

Neural Mechanism

Intrinsic ReflexesBaroreceptors (pressure sensitive receptors)Carotid, AorticChemoreceptors (located in baroreceptors)Oxygen, CO2, Hydrogen Ions

Extrinsic ReflexesControl centers found outside of circulation

Humoral Mechanisms.

Renin-Angiotensin SystemJuxtaglomerular ApparatusMacula Densa Senses change in osmolarity or Na levelsRenin is Released

Vasopressin Aka (ADH)Released from the Pituitary GlandHypothalamus Is the control center

Why do we get Blood Pressure

Properties of Arterial SystemSystolic and Diastolic ComponentsBlood VolumeElastic PropertiesCardiac OutputPeripheral 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 SystemRenin (hormone) release by juxtaglomerular cells in kidneyIncrease in sympathetic nervous system activityDecrease in MAP, Blood Pressure

Angiotensinogen gets converted in the presence of Renin to Angiotensin I

Angiotensin I Angiotensin IIVia ACE in endothelial cells in the pulmonary system

Vascular Volume &Arterial Blood Pressure Goes up

Angiotensin II

Potent VasoconstricterIncrease Na reabsorption in proximal tubule of nephron (kidneys)Stimulate the release of AldosteroNeSalt and Water reabsorption in the Collecting Ducts in the KidneyVassopressin (ADH) released from posterior pituitary in response to decreas in BP and increase in osmolarity of plasmaVasoconstrictor 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

DirectCardiac output

IndirectAutoregulationBlood flow to various tissues according to their needs

Increase renal retention of fluids

Increase Na and H20 input

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.)118

HTN - HypertensionEssential HypertensionCause?? chronic elevation in blood pressure that occurs without evidence of other diseaseessential hypertension is thought to include constitutional and environmental factors

Consequencesleft ventricular hypertrophy and heart failure, and on the vessels of the arterial system, leading to atherosclerosis, kidney disease, retinopathy, and stroke

Classification of BPSystolicDiastolic

Normal < 120< 80F/U 2 yrsPre HTN120-13980-89F/U 1 yrsStage 1 HTN140-15990-99F/U 2 moStage 2 HTN> 160> 100

Risk Factors

Family History

Age-Related Changes in Blood Pressure.

Race (more severe in african americans)

Insulin Resistance and Metabolic AbnormalitiesIncreases CAD 4X

Risk Factors

Lifestyle Risk FactorsHigh Salt Intake.Obesity. (Syndrome X) (angiotensinogen/leptin/increase aldosterone)Excess Alcohol Consumption Dietary Intake of Potassium, Calcium, and Magnesium.

Target-Organ Damage

HeartHypertrophyBrainStroke, dementia and cognitive impairmentKidneyNephrosclerosisRetinal ComplicationsRetinopathy, Vascular Hemorrhages

Treatment

JNC 7 report contains a treatment algorithmNext Slide, review

Secondary hypertension

Lifestyle Modification.

Treatment

Diuretics- Adrenergics blockersACE Inhibitors (cough)Inhibit bradykininARBCalcium Channel Receptor Blocking Drug1 receptor antagonist2 receptor agonist (clonidine)

Treatment Strategies

A regimen that helps with adherence

Side effectsNumber of doses to take

Circadian VariationDippers versus non dippersDippers exhibit normal variations

Non-dippers may have an underlying diseaseMalignant HypertensionCushingsPre-eclampsiaOrthostatic HypotensionCongestive 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 DrugsIncrease 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 BPSalt and Water resabsorption in kidneyAldosterone levels increased

May need K Sparing DiuereticsSpironolactone (Aldosterone antaganist)Blocks Principal Cells in Collecting Ducts

PheochromocytomaTumor of Chromaffin tissue (adrenal medulla)Can arise in sympathetic gangliaCatecholamine's, Epinephrine and Norepinephrine

SymptomsHeadache, palpitations, excessive sweating

50% paroxysmal50% Sustained

Diagnostic Tests

Urinary Catecholamines and their metabolitesPlasma Catecholamines

Tx:Tumor must be located and removedIf unresectable Tx with drug to block

Coarctation of the Aorta

Narrowing just distal to the sublcavian arteries

Blood flow to lower parts of body reducedIncluding kidneyActivates R-A Pathway due to decrease BPPressure 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 PressureDiastolic Values greater than 120 mmHgIntense spasms of cerebral arteriesHypertensive EncephalopathyPapilledema (on opthalmascopic examination)Injury to arteriole walls if untreated

Tx : Emergency! Partial reduction of BP

High Blood Pressure in PregnancyClassificationPreeclampsia-Eclampsia.After 1st 20 wks, proteinuria HELLP SyndromeGestational Hypertension.BP increased, without proteinuria, returns to normal 12 week postpartumChronic Hypertension.BP elevated > 140 systolic, persists after pregnancyPreeclampsia Superimposed on Chronic Hypertension.BP > 140 systolic, with proteinuria

Diagnosis and Treatment

Early Prenatal care is essential

Preeclampsia, delivery of fetus is curativeDepends on timingSurvival 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 thisObesity and decreased exerciseReview 23-4

Mostly due to secondary causesCoarctation of aorta, kidney abnormalitiesEndocrine, Pheochromocytoma or Cortisol, rareNephrotoxicity of Cyclosporine

Diagnosis and Treatment

BP should be checked once a year

Preferably non-pharmacologic treatmentLifestyle modification

Pharmacologic treatment

High Blood Pressure in the ElderlyRate of HTN increases; > 60 yrs ~50%, > 70 yrs ~ 75%Stiffening of arterial vessels, decreased baroreceptor sensitivity, increased PVRElastin fibers in walls degradePulse pressure widens

Diagnosis and TreatmentBlood PressureFollow JNC-7 same as general population

ORTHOSTATIC HYPOTENSIONPathophysiology and Causative Factors500-700 ml of blood shifted while standingUsually transient, lasting 2-3 cardiac cyclesBaroreceptors sense change ANS, ADHMedications and disease processes in elderly

AgingDecreased Systolic, decreased sensitivity to pressure changes (baroreceptors)

ORTHOSTATIC HYPOTENSIONReduced Blood Volume.Excessive use of diuretics, vomiting, diarrhea

Bed Rest and Impaired Mobility.Reduction in plasma volume, failure of peripheral vasoconstriction

Drug-Induced HypotensionAntihypertensive DrugsPsychotropic DrugsChange drug or reduce dosage

ORTHOSTATIC HYPOTENSIONDisorders of the Autonomic Nervous System.3 types of primary ANS dysfunctionPure Autonomic FailureParkinsons Dz with Autonomic FailureMultiple System Atrophy Shy-Drager Syndrome middle to late life

The Shy-Drager syndrome usually develops in middl e to late l i fe as orthostatic hypotension associated withuncoordinated movements, urinary incontinence, constipation, and other signs of neurologic defic i tsreferable to the corticospinal, extrapyramidal, corticobulbar, and cerebellar systems.145

ORTHOSTATIC HYPOTENSION

Diagnosis and Treatment

Check BP Standing and while SupineNo change in HR (baroreceptor dysfunction)Tachycardia (hypovolemia)

Pharmocologic Tx when all other failsDrugs that act on resistance vessels

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.146

JNC 8

Coming to Journals soon in your area!!

JNC 8Available March 2010