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