Htn

HypertensionHypertension

Definition:Definition: the force exerted by the the force exerted by the blood against the walls of the bleed blood against the walls of the bleed vessels vessels

Adequate to maintain tissue perfusion Adequate to maintain tissue perfusion during activity and restduring activity and rest

Arterial blood pressure: primary Arterial blood pressure: primary function of cardiac output and function of cardiac output and systemic vascular resistancesystemic vascular resistance

HypertensionHypertension

Arterial BP = Cardiac Output (CO) x Arterial BP = Cardiac Output (CO) x Systemic Systemic vascular resistance vascular resistance (SVR)(SVR)

Cardiac OutputCardiac Output = stroke volume x beats per min = stroke volume x beats per min

Systemic vascular resistanceSystemic vascular resistance = force opposing = force opposing the movement of blood within the blood vesselsthe movement of blood within the blood vessels

What is the effect on BP if SVR increased What is the effect on BP if SVR increased and CO remains constant?and CO remains constant?

HypertensionHypertension Mechanisms that Regulate Mechanisms that Regulate

BPBP

Sympathetic Nervous Sympathetic Nervous SystemSystem

Vascular EndotheliumVascular Endothelium

Renal SystemRenal System

Endocrine SystemEndocrine System

HypertensionHypertensionMechanisms that Regulate Mechanisms that Regulate

BPBPSympathetic Nervous System (SNS)Sympathetic Nervous System (SNS) – – norepinephrine released from norepinephrine released from sympathetic nerve endings - to receptors sympathetic nerve endings - to receptors alpha1, alpha2, beta 1 & beta2alpha1, alpha2, beta 1 & beta2

Reacts within secondsReacts within secondsIncreases Heart Rate - chronotropicIncreases Heart Rate - chronotropicIncreased cardiac contractility - Increased cardiac contractility - inotropicinotropic

Produces widespread vasoconstriction Produces widespread vasoconstriction in peripheral arteriolesin peripheral arterioles

Promotes release of renin from the Promotes release of renin from the kidneykidney

HypertensionHypertensionSNS Receptors Influencing B/P


BPBPSympathetic Nervous System (SNS)Sympathetic Nervous System (SNS)––

Sympathetic Vasomotor Center – located Sympathetic Vasomotor Center – located in the medulla – interacts with many areas in the medulla – interacts with many areas of the brain to maintain BP within normal of the brain to maintain BP within normal range under various conditionsrange under various conditions

Exercise – changes to meet oxygen demandExercise – changes to meet oxygen demandPostural Changes – peripheral vasoconstrictionPostural Changes – peripheral vasoconstriction


BPBPSympathetic Nervous Sympathetic Nervous System (SNS)System (SNS) – –

BaroreceptorsBaroreceptors: specialized nerve cells : specialized nerve cells the carotid arteries and the aortic archthe carotid arteries and the aortic arch

Sensitive to BP changes:Sensitive to BP changes:Increase: Inhibits SNSIncrease: Inhibits SNS – peripheral vessel – peripheral vessel

dilation. Decreased heart rate, and dilation. Decreased heart rate, and decreased contractility of the heart + decreased contractility of the heart + increased parasympathetic activity (vagus increased parasympathetic activity (vagus nerve) decreased heart ratenerve) decreased heart rate

Decrease: Activates SNSDecrease: Activates SNS – peripheral – peripheral vessel constriction, increased heart rate, vessel constriction, increased heart rate, and increased contractility of the heartand increased contractility of the heart

HypertensionHypertension Mechanisms that Regulate Mechanisms that Regulate

BPBPVascular EndotheliumVascular Endothelium

Single cell layer that lines the blood vesselsSingle cell layer that lines the blood vesselsProduce vasoactive substancesProduce vasoactive substances::

EDRF Endothelium-derive relaxing factorEDRF Endothelium-derive relaxing factor – – Helps maintain low arterial tone at restHelps maintain low arterial tone at rest Inhibits growth of the smooth muscle layerInhibits growth of the smooth muscle layer Inhibits platelet aggregationInhibits platelet aggregation

Vasodilation – prostacyclinVasodilation – prostacyclinEndothelin (ET) potent vasoconstrictor Endothelin (ET) potent vasoconstrictor

Endothelial dysfunction may contribute Endothelial dysfunction may contribute to atherosclerosis & primary to atherosclerosis & primary

hypertensionhypertension


BPBPRenal System Renal System Control Na+ excretion & extracellular Control Na+ excretion & extracellular

fluid volumefluid volumeRenal - Renin-angiotensin-aldosteroneRenal - Renin-angiotensin-aldosterone

Renin converts angiotensinogen to Renin converts angiotensinogen to angiotensin Iangiotensin I

Angiotensin-converting enzyme (ACE) Angiotensin-converting enzyme (ACE) converts I into angiotsensin II converts I into angiotsensin II Immediate: Vasoconstrictor – increased Immediate: Vasoconstrictor – increased

systemic vascular resistancesystemic vascular resistanceProlonged: Stimulates the adrenal cortex Prolonged: Stimulates the adrenal cortex

to secret Aldosterone – Na+ and Water to secret Aldosterone – Na+ and Water retentionretention

Renal MedullaRenal Medulla - Prostaglandins - - Prostaglandins - vasodilator effectvasodilator effect

HypertensionHypertensionRenin-AngiotensinRenin-Angiotensin

HypertensionHypertensionRenin-Angiotensin SystemRenin-Angiotensin System


BPBPEndocrine System Endocrine System

Stimulates the SNS with Stimulates the SNS with Epinephrine – increases HR and contractilityEpinephrine – increases HR and contractilityActivates B2-adrenergic receptors in peripheral Activates B2-adrenergic receptors in peripheral

arterioles of skeletal muscle = vasodilation arterioles of skeletal muscle = vasodilation Activates A1-adrenergic receptors in peripheral Activates A1-adrenergic receptors in peripheral

arterioles of skin and kidneys = arterioles of skin and kidneys = vasoconstictionvasoconstiction

Adrenal Cortex – Aldosterone – stimulates Adrenal Cortex – Aldosterone – stimulates kidneys to retain Na+kidneys to retain Na+

Increased Na+ stimulates posterior Increased Na+ stimulates posterior pituitary – ADH – reabsorbs ECF/waterpituitary – ADH – reabsorbs ECF/water

HypertensionHypertensionAldosterone MechanismAldosterone Mechanism

• Increased Aldosterone =Increased Aldosterone =• Increases sodium Increases sodium

reabsorption =reabsorption =• Increases water Increases water

reabsorption =reabsorption =• Increases blood volume = Increases blood volume = • Increases cardiac output Increases cardiac output


BPBP Regulatory mechanisms in the health person Regulatory mechanisms in the health person

function in response to the demands on the bodyfunction in response to the demands on the body

When Hypertension develops, one or more of When Hypertension develops, one or more of these mechanisms are defectivethese mechanisms are defective

Sympathetic Nervous SystemSympathetic Nervous System

Vascular EndotheliumVascular Endothelium

Renal SystemRenal System

Endocrine SystemEndocrine System

Secondary HypertensionSecondary HypertensionPathophysiologyPathophysiology

Specific cause of hypertension can be Specific cause of hypertension can be identifiedidentified

5+% of adult hypertension5+% of adult hypertension Causes:Causes:

Coarctation or congenital narrowing of the aortaCoarctation or congenital narrowing of the aorta Renal disease – renal artery disease / Renal disease – renal artery disease /

parenchymal parenchymal Endocrine disorders: Pheochromocytoma, Endocrine disorders: Pheochromocytoma,

Cushing Syndrome, HyperaldosteronismCushing Syndrome, Hyperaldosteronism Neurology disorders – brain tumors / head injuryNeurology disorders – brain tumors / head injury Sleep apneaSleep apnea Medications – sympathetic stimulantsMedications – sympathetic stimulants Pregnancy-induced hypertensionPregnancy-induced hypertension

HypertensionHypertensionPathophysiologyPathophysiology

Primary (Essential) Hypertension: Primary (Essential) Hypertension:

Elevated BP without an identified causeElevated BP without an identified causeAccounts for 95% of all cases of Accounts for 95% of all cases of

hypertensionhypertensionCause – unknown Cause – unknown

Contributing Factors: Contributing Factors: Increased SNS Increased SNS activity, overproduction of Na+ retaining activity, overproduction of Na+ retaining hormones & vasoconstrictors, increased Na+ hormones & vasoconstrictors, increased Na+ intake intake

Risk Factors: Risk Factors: Modifiable Modifiable

Primary HypertensionPrimary HypertensionPathophysiologyPathophysiology

Heredity Heredity – interaction of genetic, – interaction of genetic, environmental, and demographic environmental, and demographic factorsfactors

Water & Sodium RetentionWater & Sodium Retention – 20% of – 20% of pts with high Na+ diet develop HTNpts with high Na+ diet develop HTN

Altered Renin-Angiotensin Altered Renin-Angiotensin MechanismMechanism – found in 20% of patients – found in 20% of patients

Stress & Increased SNS ActivityStress & Increased SNS Activity Insulin Resistance & Insulin Resistance &

HyperinsulinemiaHyperinsulinemia Endothelial Cell DysfunctionEndothelial Cell Dysfunction

HypertensionHypertensionClinical ManifestationClinical Manifestation

Dx is made after multiple readings over Dx is made after multiple readings over several weeksseveral weeks

NIH/Joint Committee Definition:NIH/Joint Committee Definition:

CategoryCategory SystolicSystolic Diastolic DiastolicOptimalOptimal <110<110 andand < 80 < 80NormalNormal <120<120 andand <85 <85High NormalHigh Normal 130-139130-139 or or 85-89 85-89

Stage 1 140-159 140-159 or or 90-99 90-99Stage 2Stage 2 160-179160-179 oror 100-109 100-109Stage 3Stage 3 =>180=>180 oror => 110 => 110

Primary HypertensionPrimary HypertensionRisk FactorsRisk Factors

AgeAge AlcoholAlcohol Cigarette SmokingCigarette Smoking Diabetes MellitusDiabetes Mellitus Elevated serum lipidsElevated serum lipids Excess Na+ in dietExcess Na+ in diet GenderGender Family HistoryFamily History ObesityObesity EthnicityEthnicity Sedentary LifestyleSedentary Lifestyle Socioeconomic Socioeconomic StressStress

Primary HypertensionPrimary HypertensionClinical ManifestationsClinical Manifestations

Target Organ ComplicationsTarget Organ Complications::

MyocardiumMyocardium – angina / left ventricular hypertrophy – angina / left ventricular hypertrophy

BrainBrain – TIA / CVA – TIA / CVA

Peripheral vascularPeripheral vascular – Peripheral pulse change – Peripheral pulse change

KidneyKidney – renal failure Creatinine / Proteinuria – renal failure Creatinine / Proteinuria

EyesEyes – Hemorrhages with or without papilledema – Hemorrhages with or without papilledema

Primary HypertensionPrimary HypertensionClinical ManifestationsClinical Manifestations

““Silent Killer”Silent Killer” – asymptomatic and – asymptomatic and insidiousinsidious

Severe HTNSevere HTN – fatigue, reduced – fatigue, reduced activity tolerance, dyspnea, activity tolerance, dyspnea, dizziness, palpitations, angina dizziness, palpitations, angina

HypertensionHypertensionMedical DiagnosisMedical Diagnosis

History and Physical History and Physical ExaminationExamination

Renal FunctionRenal FunctionSerum Creatinine & Urine Serum Creatinine & Urine

Creatinine ClearanceCreatinine ClearanceElectrolytes – especially K+Electrolytes – especially K+Blood Glucose Blood Glucose Serum Lipids/EKGSerum Lipids/EKGAmbulatory BP MonitoringAmbulatory BP Monitoring

Primary HypertensionPrimary HypertensionMedical ManagementMedical Management

Risk StratificationRisk Stratification

Level of BPLevel of BP

Presence of Target Organ Presence of Target Organ DiseaseDisease

Other Risk FactorsOther Risk Factors

HypertensionHypertensionMedical ManagementMedical Management

Risk StratificationRisk Stratification

Primary HypertensionPrimary HypertensionMedical ManagementMedical Management

Lifestyle modificationLifestyle modification

Nutritional therapyNutritional therapy Alcohol consumptionAlcohol consumption Physical activityPhysical activity Tobacco avoidanceTobacco avoidance Stress managementStress management

Drug TherapyDrug Therapy

HypertensionHypertension NutritionNutrition

HypertensionHypertensionRisk Factor ModificationRisk Factor Modification

Primary HypertensionPrimary HypertensionMedical ManagementMedical ManagementStepped ApproachStepped Approach

Lifestyle modificationLifestyle modificationNot at Goal BPNot at Goal BP

Drug TherapyDrug TherapyNot at Goal BPNot at Goal BP

Substitute med / add a 2nd med/ Substitute med / add a 2nd med/ increase doseincrease dose

Not at Goal BPNot at Goal BP

Continue adding / changing meds until Continue adding / changing meds until controlcontrol

Primary HypertensionPrimary HypertensionMedical Management – Drug Medical Management – Drug

TherapyTherapy DiureticsDiuretics

ThiazideThiazide LoopLoop K+ SparingK+ Sparing

Adrenergic Blockers/ InhibitorsAdrenergic Blockers/ Inhibitors B-Adrenergic BlockersB-Adrenergic Blockers Central Acting Adrenergic AntagonistsCentral Acting Adrenergic Antagonists Peripheral Acting Adrenergic Peripheral Acting Adrenergic

AntagonistsAntagonists A-Adrenergic BlockersA-Adrenergic Blockers

VasodilatorsVasodilators Angiotensin InhibitorsAngiotensin Inhibitors Calcium Channel BlockersCalcium Channel Blockers

HypertensionHypertensionMedication - DiureticsMedication - Diuretics

HypertensionHypertensionMedication – Beta-blocking Medication – Beta-blocking

AgentsAgents

HypertensionHypertensionMedication Medication

Calcium Channel BlockersCalcium Channel Blockers

Hypertension Hypertension MedicationMedication

Alpha Agonists & Alpha Agonists & VasodilatorsVasodilators

HypertensionHypertensionAntihypertensive Drug Antihypertensive Drug

TherapyTherapy

Primary HypertensionPrimary HypertensionLack of Responsiveness to Lack of Responsiveness to

TherapyTherapy Nonadherence to TherapyNonadherence to Therapy

Drug-Related CausesDrug-Related Causes

Associated conditionsAssociated conditions

Secondary HypertensionSecondary Hypertension

Volume overloadVolume overload

Primary HypertensionPrimary HypertensionHypertensive CrisisHypertensive Crisis

DefinitionDefinition: Severe & abrupt elevation : Severe & abrupt elevation of BP with diastolic > 120-130mm Hg.of BP with diastolic > 120-130mm Hg.

CausesCauses::Nonadherence, renovascular changes, Nonadherence, renovascular changes,

pre- eclampsia, eclampsia, pre- eclampsia, eclampsia, Pheochromocytoma, Rebound from Pheochromocytoma, Rebound from abruptly stopping beta blockers, head abruptly stopping beta blockers, head injury, necrotizing vasculitis, acute injury, necrotizing vasculitis, acute aortic dissectionaortic dissection

Hypertensive Encephalopathy:Hypertensive Encephalopathy:headache, N/V, confusion, obtunded, headache, N/V, confusion, obtunded,

stuporous, seizures, blurred vision, stuporous, seizures, blurred vision, transient blindness transient blindness

Primary HypertensionPrimary HypertensionNursing DiagnosesNursing Diagnoses

Assess:Assess: Cardiovascular status; adherence to Cardiovascular status; adherence to therapy; family interaction; risk factor therapy; family interaction; risk factor modification?modification?

Nsg Action: Nsg Action: Supportive & reality-based; Supportive & reality-based; Administer meds; referrals; diagnostic Administer meds; referrals; diagnostic preps; preps; ask questions;ask questions;

supportive care during hospitalization for supportive care during hospitalization for acute crisisacute crisis

Pt/Family Education: Pt/Family Education: Medications; risk factor Medications; risk factor modification; Community supportmodification; Community support

HypertensionHypertensionDynamics of TreatmentDynamics of Treatment

Primary HypertensionPrimary HypertensionCase StudyCase Study

Health & Medicine

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