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HYPERTENSIONHYPERTENSION
Lecture byLecture by
Dr.Nasim AhmedDr.Nasim Ahmed
DEPARTMENT OFDEPARTMENT OF
ANAESTHESIAANAESTHESIA
SIUTSIUT
HypertensionHypertension
Definition:Definition: the force exerted by the bloodthe force exerted by the blood
against the walls of the bleed vesselsagainst the walls of the bleed vessels
Adequate to maintain tissue perfusion duringAdequate to maintain tissue perfusion during
activity and restactivity and rest
Arterial blood pressure: primary function ofArterial blood pressure: primary function of
cardiac output and systemic vascular resistancecardiac output and systemic vascular resistance
HypertensionHypertension
Arterial BP = Cardiac Output (CO) x SystemicArterial BP = Cardiac Output (CO) x Systemic
vascular resistance (SVR)vascular resistance (SVR)
Cardiac OutputCardiac Output = stroke volume x beats per min= stroke volume x beats per min
Systemic vascular resistanceSystemic vascular resistance = force opposing the= force opposing the
movement of blood within the blood vesselsmovement of blood within the blood vessels
What is the effect on BP if SVR increased and COWhat is the effect on BP if SVR increased and CO
remains constant?remains constant?
HypertensionHypertension
Mechanisms that Regulate BPMechanisms that Regulate BP
Sympathetic Nervous SystemSympathetic Nervous System
Vascular EndotheliumVascular Endothelium
Renal SystemRenal System
Endocrine SystemEndocrine System
HypertensionHypertension
Mechanisms that Regulate BPMechanisms that Regulate BP
Sympathetic Nervous System (SNS)Sympathetic Nervous System (SNS) ––
norepinephrine released from sympathetic nervenorepinephrine released from sympathetic nerve
endings - to receptors alpha1, alpha2, beta 1 & beta2endings - to receptors alpha1, alpha2, beta 1 & beta2
Reacts within secondsReacts within seconds
Increases Heart Rate - chronotropicIncreases Heart Rate - chronotropic
Increased cardiac contractility - inotropicIncreased cardiac contractility - inotropic
Produces widespread vasoconstriction inProduces widespread vasoconstriction in
peripheral arteriolesperipheral arterioles
Promotes release of renin from the kidneyPromotes release of renin from the kidney
HypertensionHypertension
SNS Receptors Influencing B/P
HypertensionHypertension
Mechanisms that Regulate BPMechanisms that Regulate BP
Sympathetic Nervous System (SNS)Sympathetic Nervous System (SNS)––
Sympathetic Vasomotor Center – located in theSympathetic Vasomotor Center – located in the
medulla – interacts with many areas of the brainmedulla – interacts with many areas of the brain
to maintain BP within normal range underto maintain BP within normal range under
various conditionsvarious conditions
Exercise – changes to meet oxygen demandExercise – changes to meet oxygen demand
Postural Changes – peripheral vasoconstrictionPostural Changes – peripheral vasoconstriction
HypertensionHypertension
Mechanisms that Regulate BPMechanisms that Regulate BP
Sympathetic NervousSympathetic Nervous System (SNS)System (SNS) ––
BaroreceptorsBaroreceptors: specialized nerve cells the carotid: specialized nerve cells the carotid
arteries and the aortic archarteries and the aortic arch
Sensitive to BP changes:Sensitive to BP changes:
Increase: Inhibits SNSIncrease: Inhibits SNS – peripheral vessel dilation.– peripheral vessel dilation.
Decreased heart rate, and decreased contractility ofDecreased heart rate, and decreased contractility of
the heart + increased parasympathetic activity (vagusthe heart + increased parasympathetic activity (vagus
nerve) decreased heart ratenerve) decreased heart rate
Decrease: Activates SNSDecrease: Activates SNS – peripheral vessel– peripheral vessel
constriction, increased heart rate, and increasedconstriction, increased heart rate, and increased
contractility of the heartcontractility of the heart
HypertensionHypertension
Mechanisms that Regulate BPMechanisms that Regulate BP
Vascular EndotheliumVascular Endothelium
Single cell layer that lines the blood vesselsSingle cell layer that lines the blood vessels
Produce 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 – prostacyclin
Endothelin (ET) potent vasoconstrictorEndothelin (ET) potent vasoconstrictor
Endothelial dysfunction may contribute toEndothelial dysfunction may contribute to
atherosclerosis & primary hypertensionatherosclerosis & primary hypertension
HypertensionHypertension
Mechanisms that Regulate BPMechanisms that Regulate BP
Renal SystemRenal System
Control Na+ excretion & extracellular fluidControl Na+ excretion & extracellular fluid
volumevolume
Renal - Renin-angiotensin-aldosteroneRenal - Renin-angiotensin-aldosterone
Renin converts angiotensinogen to angiotensin IRenin converts angiotensinogen to angiotensin I
Angiotensin-converting enzyme (ACE) converts I intoAngiotensin-converting enzyme (ACE) converts I into
angiotsensin IIangiotsensin II
Immediate: Vasoconstrictor – increased systemicImmediate: Vasoconstrictor – increased systemic
vascular resistancevascular resistance
Prolonged: Stimulates the adrenal cortex to secretProlonged: Stimulates the adrenal cortex to secret
Aldosterone – Na+ and Water retentionAldosterone – Na+ and Water retention
Renal MedullaRenal Medulla - Prostaglandins - vasodilator effect- Prostaglandins - vasodilator effect
HypertensionHypertension
Renin-AngiotensinRenin-Angiotensin
HypertensionHypertension
Renin-Angiotensin SystemRenin-Angiotensin System
HypertensionHypertension
Mechanisms that Regulate BPMechanisms that Regulate BP
Endocrine SystemEndocrine System
Stimulates the SNS withStimulates the SNS with
Epinephrine – increases HR and contractilityEpinephrine – increases HR and contractility
Activates B2-adrenergic receptors in peripheral arterioles ofActivates B2-adrenergic receptors in peripheral arterioles of
skeletal muscle = vasodilationskeletal muscle = vasodilation
Activates A1-adrenergic receptors in peripheral arterioles ofActivates A1-adrenergic receptors in peripheral arterioles of
skin and kidneys = vasoconstictionskin and kidneys = vasoconstiction
Adrenal Cortex – Aldosterone – stimulates kidneys toAdrenal Cortex – Aldosterone – stimulates kidneys to
retain Na+retain Na+
Increased Na+ stimulates posterior pituitary – ADH –Increased Na+ stimulates posterior pituitary – ADH –
reabsorbs ECF/waterreabsorbs ECF/water
HypertensionHypertension
Aldosterone MechanismAldosterone Mechanism
• Increased Aldosterone =Increased Aldosterone =
• Increases sodium reabsorption =Increases sodium reabsorption =
• Increases water reabsorption =Increases water reabsorption =
• Increases blood volume =Increases blood volume =
• Increases cardiac outputIncreases cardiac output
HypertensionHypertension
Mechanisms that Regulate BPMechanisms that Regulate BP
 Regulatory mechanisms in the health person function in responseRegulatory mechanisms in the health person function in response
to the demands on the bodyto the demands on the body
 When Hypertension develops, one or more of these mechanismsWhen Hypertension develops, one or more of these mechanisms
are defectiveare defective
Sympathetic Nervous SystemSympathetic Nervous System
Vascular EndotheliumVascular Endothelium
Renal SystemRenal System
Endocrine SystemEndocrine System
Secondary HypertensionSecondary Hypertension
PathophysiologyPathophysiology
 Specific cause of hypertension can be identifiedSpecific cause of hypertension can be identified
 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 / parenchymalRenal disease – renal artery disease / parenchymal
 Endocrine disorders: Pheochromocytoma, CushingEndocrine disorders: Pheochromocytoma, Cushing
Syndrome, HyperaldosteronismSyndrome, 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
HypertensionHypertension
PathophysiologyPathophysiology
Primary (Essential) Hypertension:Primary (Essential) Hypertension:
Elevated BP without an identified causeElevated BP without an identified cause
Accounts for 95% of all cases of hypertensionAccounts for 95% of all cases of hypertension
Cause – unknownCause – unknown
Contributing Factors:Contributing Factors: Increased SNS activity,Increased SNS activity,
overproduction of Na+ retaining hormones &overproduction of Na+ retaining hormones &
vasoconstrictors, increased Na+ intakevasoconstrictors, increased Na+ intake
Risk Factors:Risk Factors: ModifiableModifiable
Primary HypertensionPrimary Hypertension
PathophysiologyPathophysiology
HeredityHeredity – interaction of genetic,– interaction of genetic,
environmental, and demographic factorsenvironmental, and demographic factors
Water & Sodium RetentionWater & Sodium Retention – 20% of pts– 20% of pts
with high Na+ diet develop HTNwith high Na+ diet develop HTN
Altered Renin-Angiotensin MechanismAltered Renin-Angiotensin Mechanism ––
found in 20% of patientsfound in 20% of patients
 Stress & Increased SNS ActivityStress & Increased SNS Activity
Insulin Resistance & HyperinsulinemiaInsulin Resistance & Hyperinsulinemia
Endothelial Cell DysfunctionEndothelial Cell Dysfunction
HypertensionHypertension
Clinical ManifestationClinical Manifestation
Dx is made after multiple readings over several weeksDx is made after multiple readings over several weeks
NIH/Joint Committee Definition:NIH/Joint Committee Definition:
CategoryCategory SystolicSystolic DiastolicDiastolic
OptimalOptimal <110<110 andand < 80< 80
NormalNormal <120<120 andand <85<85
High NormalHigh Normal 130-139130-139 oror 85-8985-89
Stage 1 140-159140-159 oror 90-9990-99
Stage 2Stage 2 160-179160-179 oror 100-109100-109
Stage 3Stage 3 =>180=>180 oror => 110=> 110
Primary HypertensionPrimary Hypertension
Risk 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
 SocioeconomicSocioeconomic
 StressStress
Primary HypertensionPrimary Hypertension
Clinical 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 Hypertension
Clinical ManifestationsClinical Manifestations
““Silent Killer”Silent Killer” – asymptomatic and insidious– asymptomatic and insidious
Severe HTNSevere HTN – fatigue, reduced activity– fatigue, reduced activity
tolerance, dyspnea, dizziness, palpitations,tolerance, dyspnea, dizziness, palpitations,
anginaangina
HypertensionHypertension
Medical DiagnosisMedical Diagnosis
History and Physical ExaminationHistory and Physical Examination
Renal FunctionRenal Function
Serum Creatinine & Urine CreatinineSerum Creatinine & Urine Creatinine
ClearanceClearance
Electrolytes – especially K+Electrolytes – especially K+
Blood GlucoseBlood Glucose
Serum Lipids/EKGSerum Lipids/EKG
Ambulatory BP MonitoringAmbulatory BP Monitoring
Primary HypertensionPrimary Hypertension
Medical ManagementMedical Management
Risk StratificationRisk Stratification
Level of BPLevel of BP
Presence of Target Organ DiseasePresence of Target Organ Disease
Other Risk FactorsOther Risk Factors
HypertensionHypertension
Medical ManagementMedical Management
Risk StratificationRisk Stratification
Primary HypertensionPrimary Hypertension
Medical 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
HypertensionHypertension
Risk Factor ModificationRisk Factor Modification
Primary HypertensionPrimary Hypertension
Medical ManagementMedical Management
Stepped ApproachStepped Approach
Lifestyle modificationLifestyle modification
Not at Goal BPNot at Goal BP
Drug TherapyDrug Therapy
Not at Goal BPNot at Goal BP
Substitute med / add a 2nd med/ increase doseSubstitute med / add a 2nd med/ increase dose
Not at Goal BPNot at Goal BP
Continue adding / changing meds until controlContinue adding / changing meds until control
Primary HypertensionPrimary Hypertension
Medical Management – Drug TherapyMedical Management – Drug Therapy
 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 AntagonistsPeripheral Acting Adrenergic Antagonists
 A-Adrenergic BlockersA-Adrenergic Blockers
 VasodilatorsVasodilators
 Angiotensin InhibitorsAngiotensin Inhibitors
 Calcium Channel BlockersCalcium Channel Blockers
HypertensionHypertension
Medication - DiureticsMedication - Diuretics
HypertensionHypertension
Medication – Beta-blocking AgentsMedication – Beta-blocking Agents
HypertensionHypertension
MedicationMedication
Calcium Channel BlockersCalcium Channel Blockers
HypertensionHypertension
MedicationMedication
Alpha Agonists & VasodilatorsAlpha Agonists & Vasodilators
HypertensionHypertension
Antihypertensive Drug TherapyAntihypertensive Drug Therapy
Primary HypertensionPrimary Hypertension
Lack of Responsiveness to TherapyLack of Responsiveness to Therapy
 Nonadherence to TherapyNonadherence to Therapy
 Drug-Related CausesDrug-Related Causes
 Associated conditionsAssociated conditions
 Secondary HypertensionSecondary Hypertension
 Volume overloadVolume overload
Primary HypertensionPrimary Hypertension
Hypertensive CrisisHypertensive Crisis
DefinitionDefinition: Severe & abrupt elevation of BP with: Severe & abrupt elevation of BP with
diastolic > 120-130mm Hg.diastolic > 120-130mm Hg.
CausesCauses::
Nonadherence, renovascular changes, pre-Nonadherence, renovascular changes, pre-
eclampsia, eclampsia, Pheochromocytoma,eclampsia, eclampsia, Pheochromocytoma,
Rebound from abruptly stopping beta blockers,Rebound from abruptly stopping beta blockers,
head injury, necrotizing vasculitis, acute aortichead injury, necrotizing vasculitis, acute aortic
dissectiondissection
Hypertensive Encephalopathy:Hypertensive Encephalopathy:
headache, N/V, confusion, obtunded, stuporous,headache, N/V, confusion, obtunded, stuporous,
seizures, blurred vision, transient blindnessseizures, blurred vision, transient blindness
Primary HypertensionPrimary Hypertension
Nursing DiagnosesNursing Diagnoses
Assess:Assess: Cardiovascular status; adherence to therapy; familyCardiovascular status; adherence to therapy; family
interaction; risk factor modification?interaction; risk factor modification?
Nsg Action:Nsg Action: Supportive & reality-based; Administer meds;Supportive & reality-based; Administer meds;
referrals; diagnostic preps;referrals; diagnostic preps; ask questions;ask questions;
supportive care during hospitalization for acute crisissupportive care during hospitalization for acute crisis
Pt/Family Education:Pt/Family Education: Medications; risk factorMedications; risk factor
modification; Community supportmodification; Community support
HypertensionHypertension
Dynamics of TreatmentDynamics of Treatment
Primary HypertensionPrimary Hypertension
Case StudyCase Study
THANK YOUTHANK YOU

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Hypertension Lecture Summary by Dr. Nasim Ahmed

  • 1. HYPERTENSIONHYPERTENSION Lecture byLecture by Dr.Nasim AhmedDr.Nasim Ahmed DEPARTMENT OFDEPARTMENT OF ANAESTHESIAANAESTHESIA SIUTSIUT
  • 2. HypertensionHypertension Definition:Definition: the force exerted by the bloodthe force exerted by the blood against the walls of the bleed vesselsagainst the walls of the bleed vessels Adequate to maintain tissue perfusion duringAdequate to maintain tissue perfusion during activity and restactivity and rest Arterial blood pressure: primary function ofArterial blood pressure: primary function of cardiac output and systemic vascular resistancecardiac output and systemic vascular resistance
  • 3. HypertensionHypertension Arterial BP = Cardiac Output (CO) x SystemicArterial BP = Cardiac Output (CO) x Systemic vascular resistance (SVR)vascular resistance (SVR) Cardiac OutputCardiac Output = stroke volume x beats per min= stroke volume x beats per min Systemic vascular resistanceSystemic vascular resistance = force opposing the= force opposing the movement of blood within the blood vesselsmovement of blood within the blood vessels What is the effect on BP if SVR increased and COWhat is the effect on BP if SVR increased and CO remains constant?remains constant?
  • 4. HypertensionHypertension Mechanisms that Regulate BPMechanisms that Regulate BP Sympathetic Nervous SystemSympathetic Nervous System Vascular EndotheliumVascular Endothelium Renal SystemRenal System Endocrine SystemEndocrine System
  • 5. HypertensionHypertension Mechanisms that Regulate BPMechanisms that Regulate BP Sympathetic Nervous System (SNS)Sympathetic Nervous System (SNS) –– norepinephrine released from sympathetic nervenorepinephrine released from sympathetic nerve endings - to receptors alpha1, alpha2, beta 1 & beta2endings - to receptors alpha1, alpha2, beta 1 & beta2 Reacts within secondsReacts within seconds Increases Heart Rate - chronotropicIncreases Heart Rate - chronotropic Increased cardiac contractility - inotropicIncreased cardiac contractility - inotropic Produces widespread vasoconstriction inProduces widespread vasoconstriction in peripheral arteriolesperipheral arterioles Promotes release of renin from the kidneyPromotes release of renin from the kidney
  • 7. HypertensionHypertension Mechanisms that Regulate BPMechanisms that Regulate BP Sympathetic Nervous System (SNS)Sympathetic Nervous System (SNS)–– Sympathetic Vasomotor Center – located in theSympathetic Vasomotor Center – located in the medulla – interacts with many areas of the brainmedulla – interacts with many areas of the brain to maintain BP within normal range underto maintain BP within normal range under various conditionsvarious conditions Exercise – changes to meet oxygen demandExercise – changes to meet oxygen demand Postural Changes – peripheral vasoconstrictionPostural Changes – peripheral vasoconstriction
  • 8. HypertensionHypertension Mechanisms that Regulate BPMechanisms that Regulate BP Sympathetic NervousSympathetic Nervous System (SNS)System (SNS) –– BaroreceptorsBaroreceptors: specialized nerve cells the carotid: specialized nerve cells the carotid arteries and the aortic archarteries and the aortic arch Sensitive to BP changes:Sensitive to BP changes: Increase: Inhibits SNSIncrease: Inhibits SNS – peripheral vessel dilation.– peripheral vessel dilation. Decreased heart rate, and decreased contractility ofDecreased heart rate, and decreased contractility of the heart + increased parasympathetic activity (vagusthe heart + increased parasympathetic activity (vagus nerve) decreased heart ratenerve) decreased heart rate Decrease: Activates SNSDecrease: Activates SNS – peripheral vessel– peripheral vessel constriction, increased heart rate, and increasedconstriction, increased heart rate, and increased contractility of the heartcontractility of the heart
  • 9. HypertensionHypertension Mechanisms that Regulate BPMechanisms that Regulate BP Vascular EndotheliumVascular Endothelium Single cell layer that lines the blood vesselsSingle cell layer that lines the blood vessels Produce 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 – prostacyclin Endothelin (ET) potent vasoconstrictorEndothelin (ET) potent vasoconstrictor Endothelial dysfunction may contribute toEndothelial dysfunction may contribute to atherosclerosis & primary hypertensionatherosclerosis & primary hypertension
  • 10. HypertensionHypertension Mechanisms that Regulate BPMechanisms that Regulate BP Renal SystemRenal System Control Na+ excretion & extracellular fluidControl Na+ excretion & extracellular fluid volumevolume Renal - Renin-angiotensin-aldosteroneRenal - Renin-angiotensin-aldosterone Renin converts angiotensinogen to angiotensin IRenin converts angiotensinogen to angiotensin I Angiotensin-converting enzyme (ACE) converts I intoAngiotensin-converting enzyme (ACE) converts I into angiotsensin IIangiotsensin II Immediate: Vasoconstrictor – increased systemicImmediate: Vasoconstrictor – increased systemic vascular resistancevascular resistance Prolonged: Stimulates the adrenal cortex to secretProlonged: Stimulates the adrenal cortex to secret Aldosterone – Na+ and Water retentionAldosterone – Na+ and Water retention Renal MedullaRenal Medulla - Prostaglandins - vasodilator effect- Prostaglandins - vasodilator effect
  • 13. HypertensionHypertension Mechanisms that Regulate BPMechanisms that Regulate BP Endocrine SystemEndocrine System Stimulates the SNS withStimulates the SNS with Epinephrine – increases HR and contractilityEpinephrine – increases HR and contractility Activates B2-adrenergic receptors in peripheral arterioles ofActivates B2-adrenergic receptors in peripheral arterioles of skeletal muscle = vasodilationskeletal muscle = vasodilation Activates A1-adrenergic receptors in peripheral arterioles ofActivates A1-adrenergic receptors in peripheral arterioles of skin and kidneys = vasoconstictionskin and kidneys = vasoconstiction Adrenal Cortex – Aldosterone – stimulates kidneys toAdrenal Cortex – Aldosterone – stimulates kidneys to retain Na+retain Na+ Increased Na+ stimulates posterior pituitary – ADH –Increased Na+ stimulates posterior pituitary – ADH – reabsorbs ECF/waterreabsorbs ECF/water
  • 14. HypertensionHypertension Aldosterone MechanismAldosterone Mechanism • Increased Aldosterone =Increased Aldosterone = • Increases sodium reabsorption =Increases sodium reabsorption = • Increases water reabsorption =Increases water reabsorption = • Increases blood volume =Increases blood volume = • Increases cardiac outputIncreases cardiac output
  • 15. HypertensionHypertension Mechanisms that Regulate BPMechanisms that Regulate BP  Regulatory mechanisms in the health person function in responseRegulatory mechanisms in the health person function in response to the demands on the bodyto the demands on the body  When Hypertension develops, one or more of these mechanismsWhen Hypertension develops, one or more of these mechanisms are defectiveare defective Sympathetic Nervous SystemSympathetic Nervous System Vascular EndotheliumVascular Endothelium Renal SystemRenal System Endocrine SystemEndocrine System
  • 16. Secondary HypertensionSecondary Hypertension PathophysiologyPathophysiology  Specific cause of hypertension can be identifiedSpecific cause of hypertension can be identified  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 / parenchymalRenal disease – renal artery disease / parenchymal  Endocrine disorders: Pheochromocytoma, CushingEndocrine disorders: Pheochromocytoma, Cushing Syndrome, HyperaldosteronismSyndrome, 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
  • 17. HypertensionHypertension PathophysiologyPathophysiology Primary (Essential) Hypertension:Primary (Essential) Hypertension: Elevated BP without an identified causeElevated BP without an identified cause Accounts for 95% of all cases of hypertensionAccounts for 95% of all cases of hypertension Cause – unknownCause – unknown Contributing Factors:Contributing Factors: Increased SNS activity,Increased SNS activity, overproduction of Na+ retaining hormones &overproduction of Na+ retaining hormones & vasoconstrictors, increased Na+ intakevasoconstrictors, increased Na+ intake Risk Factors:Risk Factors: ModifiableModifiable
  • 18. Primary HypertensionPrimary Hypertension PathophysiologyPathophysiology HeredityHeredity – interaction of genetic,– interaction of genetic, environmental, and demographic factorsenvironmental, and demographic factors Water & Sodium RetentionWater & Sodium Retention – 20% of pts– 20% of pts with high Na+ diet develop HTNwith high Na+ diet develop HTN Altered Renin-Angiotensin MechanismAltered Renin-Angiotensin Mechanism –– found in 20% of patientsfound in 20% of patients  Stress & Increased SNS ActivityStress & Increased SNS Activity Insulin Resistance & HyperinsulinemiaInsulin Resistance & Hyperinsulinemia Endothelial Cell DysfunctionEndothelial Cell Dysfunction
  • 19. HypertensionHypertension Clinical ManifestationClinical Manifestation Dx is made after multiple readings over several weeksDx is made after multiple readings over several weeks NIH/Joint Committee Definition:NIH/Joint Committee Definition: CategoryCategory SystolicSystolic DiastolicDiastolic OptimalOptimal <110<110 andand < 80< 80 NormalNormal <120<120 andand <85<85 High NormalHigh Normal 130-139130-139 oror 85-8985-89 Stage 1 140-159140-159 oror 90-9990-99 Stage 2Stage 2 160-179160-179 oror 100-109100-109 Stage 3Stage 3 =>180=>180 oror => 110=> 110
  • 20. Primary HypertensionPrimary Hypertension Risk 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  SocioeconomicSocioeconomic  StressStress
  • 21. Primary HypertensionPrimary Hypertension Clinical 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
  • 22. Primary HypertensionPrimary Hypertension Clinical ManifestationsClinical Manifestations ““Silent Killer”Silent Killer” – asymptomatic and insidious– asymptomatic and insidious Severe HTNSevere HTN – fatigue, reduced activity– fatigue, reduced activity tolerance, dyspnea, dizziness, palpitations,tolerance, dyspnea, dizziness, palpitations, anginaangina
  • 23. HypertensionHypertension Medical DiagnosisMedical Diagnosis History and Physical ExaminationHistory and Physical Examination Renal FunctionRenal Function Serum Creatinine & Urine CreatinineSerum Creatinine & Urine Creatinine ClearanceClearance Electrolytes – especially K+Electrolytes – especially K+ Blood GlucoseBlood Glucose Serum Lipids/EKGSerum Lipids/EKG Ambulatory BP MonitoringAmbulatory BP Monitoring
  • 24. Primary HypertensionPrimary Hypertension Medical ManagementMedical Management Risk StratificationRisk Stratification Level of BPLevel of BP Presence of Target Organ DiseasePresence of Target Organ Disease Other Risk FactorsOther Risk Factors
  • 26. Primary HypertensionPrimary Hypertension Medical ManagementMedical Management  Lifestyle modificationLifestyle modification  Nutritional therapyNutritional therapy  Alcohol consumptionAlcohol consumption  Physical activityPhysical activity  Tobacco avoidanceTobacco avoidance  Stress managementStress management  Drug TherapyDrug Therapy
  • 29. Primary HypertensionPrimary Hypertension Medical ManagementMedical Management Stepped ApproachStepped Approach Lifestyle modificationLifestyle modification Not at Goal BPNot at Goal BP Drug TherapyDrug Therapy Not at Goal BPNot at Goal BP Substitute med / add a 2nd med/ increase doseSubstitute med / add a 2nd med/ increase dose Not at Goal BPNot at Goal BP Continue adding / changing meds until controlContinue adding / changing meds until control
  • 30. Primary HypertensionPrimary Hypertension Medical Management – Drug TherapyMedical Management – Drug Therapy  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 AntagonistsPeripheral Acting Adrenergic Antagonists  A-Adrenergic BlockersA-Adrenergic Blockers  VasodilatorsVasodilators  Angiotensin InhibitorsAngiotensin Inhibitors  Calcium Channel BlockersCalcium Channel Blockers
  • 32. HypertensionHypertension Medication – Beta-blocking AgentsMedication – Beta-blocking Agents
  • 34. HypertensionHypertension MedicationMedication Alpha Agonists & VasodilatorsAlpha Agonists & Vasodilators
  • 36. Primary HypertensionPrimary Hypertension Lack of Responsiveness to TherapyLack of Responsiveness to Therapy  Nonadherence to TherapyNonadherence to Therapy  Drug-Related CausesDrug-Related Causes  Associated conditionsAssociated conditions  Secondary HypertensionSecondary Hypertension  Volume overloadVolume overload
  • 37. Primary HypertensionPrimary Hypertension Hypertensive CrisisHypertensive Crisis DefinitionDefinition: Severe & abrupt elevation of BP with: Severe & abrupt elevation of BP with diastolic > 120-130mm Hg.diastolic > 120-130mm Hg. CausesCauses:: Nonadherence, renovascular changes, pre-Nonadherence, renovascular changes, pre- eclampsia, eclampsia, Pheochromocytoma,eclampsia, eclampsia, Pheochromocytoma, Rebound from abruptly stopping beta blockers,Rebound from abruptly stopping beta blockers, head injury, necrotizing vasculitis, acute aortichead injury, necrotizing vasculitis, acute aortic dissectiondissection Hypertensive Encephalopathy:Hypertensive Encephalopathy: headache, N/V, confusion, obtunded, stuporous,headache, N/V, confusion, obtunded, stuporous, seizures, blurred vision, transient blindnessseizures, blurred vision, transient blindness
  • 38. Primary HypertensionPrimary Hypertension Nursing DiagnosesNursing Diagnoses Assess:Assess: Cardiovascular status; adherence to therapy; familyCardiovascular status; adherence to therapy; family interaction; risk factor modification?interaction; risk factor modification? Nsg Action:Nsg Action: Supportive & reality-based; Administer meds;Supportive & reality-based; Administer meds; referrals; diagnostic preps;referrals; diagnostic preps; ask questions;ask questions; supportive care during hospitalization for acute crisissupportive care during hospitalization for acute crisis Pt/Family Education:Pt/Family Education: Medications; risk factorMedications; risk factor modification; Community supportmodification; Community support