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Hypertension. Definition: the force exerted by the blood against the walls of the bleed vessels. Adequate to maintain tissue perfusion during activity and rest ...
File link: http://www.mccc.edu/~martinl/documents/HTN.ppt



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    Hypertension Hypertension Presentation Transcript

    • Hypertension Definition: the force exerted by the blood against the walls of the bleed vessels Adequate to maintain tissue perfusion during activity and rest Arterial blood pressure: primary function of cardiac output and systemic vascular resistance
    • HypertensionArterial BP = Cardiac Output (CO) x Systemic vascular resistance (SVR)Cardiac Output = stroke volume x beats per minSystemic vascular resistance = force opposing the movement of blood within the blood vesselsWhat is the effect on BP if SVR increased and CO remains constant?
    • HypertensionMechanisms that Regulate BP  Sympathetic Nervous System  Vascular Endothelium  Renal System  Endocrine System
    • Hypertension Mechanisms that Regulate BP Sympathetic Nervous System (SNS) – norepinephrine released from sympathetic nerve endings - to receptors alpha1, alpha2, beta 1 & beta2 Reacts within seconds Increases Heart Rate - chronotropic Increased cardiac contractility - inotropic Produces widespread vasoconstriction in peripheral arterioles Promotes release of renin from the kidney
    • HypertensionSNS Receptors Influencing B/P
    • Hypertension Mechanisms that Regulate BP Sympathetic Nervous System (SNS)– Sympathetic Vasomotor Center – located in the medulla – interacts with many areas of the brain to maintain BP within normal range under various conditions Exercise – changes to meet oxygen demand Postural Changes – peripheral vasoconstriction
    • Hypertension Mechanisms that Regulate BP Sympathetic Nervous System (SNS) – Baroreceptors: specialized nerve cells the carotid arteries and the aortic arch Sensitive to BP changes: Increase: Inhibits SNS – peripheral vessel dilation. Decreased heart rate, and decreased contractility of the heart + increased parasympathetic activity (vagus nerve) decreased heart rate Decrease: Activates SNS – peripheral vessel constriction, increased heart rate, and increased contractility of the heart
    • Hypertension Mechanisms that Regulate BP Vascular Endothelium Single cell layer that lines the blood vessels Produce vasoactive substances: EDRF Endothelium-derive relaxing factor –  Helps maintain low arterial tone at rest  Inhibits growth of the smooth muscle layer  Inhibits platelet aggregation Vasodilation – prostacyclin Endothelin (ET) potent vasoconstrictor Endothelial dysfunction may contribute to atherosclerosis & primary hypertension
    • Hypertension Mechanisms that Regulate BP Renal System Control Na+ excretion & extracellular fluid volume Renal - Renin-angiotensin-aldosterone Renin converts angiotensinogen to angiotensin I Angiotensin-converting enzyme (ACE) converts I into angiotsensin II Immediate: Vasoconstrictor – increased systemic vascular resistance Prolonged: Stimulates the adrenal cortex to secret Aldosterone – Na+ and Water retention Renal Medulla - Prostaglandins - vasodilator effect
    • HypertensionRenin-Angiotensin
    • HypertensionRenin-Angiotensin System
    • Hypertension Mechanisms that Regulate BP Endocrine System Stimulates the SNS with Epinephrine – increases HR and contractility Activates B2-adrenergic receptors in peripheral arterioles of skeletal muscle = vasodilation Activates A1-adrenergic receptors in peripheral arterioles of skin and kidneys = vasoconstiction Adrenal Cortex – Aldosterone – stimulates kidneys to retain Na+ Increased Na+ stimulates posterior pituitary – ADH – reabsorbs ECF/water
    • HypertensionAldosterone Mechanism• Increased Aldosterone =• Increases sodium reabsorption =• Increases water reabsorption =• Increases blood volume =• Increases cardiac output
    • Hypertension Mechanisms that Regulate BP Regulatory mechanisms in the health person function in response to the demands on the body When Hypertension develops, one or more of these mechanisms are defective  Sympathetic Nervous System  Vascular Endothelium  Renal System  Endocrine System
    • Secondary Hypertension Pathophysiology Specific cause of hypertension can be identified 5+% of adult hypertension Causes:  Coarctation or congenital narrowing of the aorta  Renal disease – renal artery disease / parenchymal  Endocrine disorders: Pheochromocytoma, Cushing Syndrome, Hyperaldosteronism  Neurology disorders – brain tumors / head injury  Sleep apnea  Medications – sympathetic stimulants  Pregnancy-induced hypertension
    • Hypertension Pathophysiology Primary (Essential) Hypertension: Elevated BP without an identified cause Accounts for 95% of all cases of hypertension Cause – unknown Contributing Factors: Increased SNS activity, overproduction of Na+ retaining hormones & vasoconstrictors, increased Na+ intake Risk Factors: Modifiable
    • Primary Hypertension Pathophysiology Heredity – interaction of genetic, environmental, and demographic factors Water & Sodium Retention – 20% of pts with high Na+ diet develop HTN Altered Renin-Angiotensin Mechanism – found in 20% of patients Stress & Increased SNS Activity Insulin Resistance & Hyperinsulinemia Endothelial Cell Dysfunction
    • Hypertension Clinical ManifestationDx is made after multiple readings over several weeksNIH/Joint Committee Definition:Category Systolic DiastolicOptimal <110 and < 80Normal <120 and <85High Normal 130-139 or 85-89Stage 1 140-159 or 90-99Stage 2 160-179 or 100-109Stage 3 =>180 or => 110
    • Primary Hypertension Risk Factors  Age  Alcohol  Cigarette Smoking  Diabetes Mellitus  Elevated serum lipids  Excess Na+ in diet  Gender  Family History  Obesity  Ethnicity  Sedentary Lifestyle  Socioeconomic  Stress
    • Primary Hypertension Clinical Manifestations Target Organ Complications:  Myocardium – angina / left ventricular hypertrophy  Brain – TIA / CVA  Peripheral vascular – Peripheral pulse change  Kidney – renal failure Creatinine / Proteinuria  Eyes – Hemorrhages with or without papilledema
    • Primary Hypertension Clinical Manifestations “Silent Killer” – asymptomatic and insidious Severe HTN – fatigue, reduced activity tolerance, dyspnea, dizziness, palpitations, angina
    • Hypertension Medical Diagnosis History and Physical Examination Renal Function Serum Creatinine & Urine Creatinine Clearance Electrolytes – especially K+ Blood Glucose Serum Lipids/EKG Ambulatory BP Monitoring
    • Primary HypertensionMedical Management Risk Stratification Level of BP Presence of Target Organ Disease Other Risk Factors
    • HypertensionMedical Management Risk Stratification
    • Primary HypertensionMedical Management Lifestyle modification  Nutritional therapy  Alcohol consumption  Physical activity  Tobacco avoidance  Stress management Drug Therapy
    • Hypertension Nutrition
    • HypertensionRisk Factor Modification
    • Primary Hypertension Medical Management Stepped Approach Lifestyle modification Not at Goal BP Drug Therapy Not at Goal BPSubstitute med / add a 2nd med/ increase dose Not at Goal BPContinue adding / changing meds until control
    • Primary Hypertension Medical Management – Drug Therapy Diuretics  Thiazide  Loop  K+ Sparing Adrenergic Blockers/ Inhibitors  B-Adrenergic Blockers  Central Acting Adrenergic Antagonists  Peripheral Acting Adrenergic Antagonists  A-Adrenergic Blockers Vasodilators Angiotensin Inhibitors Calcium Channel Blockers
    • HypertensionMedication - Diuretics
    • HypertensionMedication – Beta-blocking Agents
    • Hypertension MedicationCalcium Channel Blockers
    • Hypertension MedicationAlpha Agonists & Vasodilators
    • HypertensionAntihypertensive Drug Therapy
    • Primary HypertensionLack of Responsiveness to Therapy  Nonadherence to Therapy  Drug-Related Causes  Associated conditions  Secondary Hypertension  Volume overload
    • Primary Hypertension Hypertensive Crisis Definition: Severe & abrupt elevation of BP with diastolic > 120-130mm Hg. Causes: Nonadherence, renovascular changes, pre- eclampsia, eclampsia, Pheochromocytoma, Rebound from abruptly stopping beta blockers, head injury, necrotizing vasculitis, acute aortic dissection Hypertensive Encephalopathy: headache, N/V, confusion, obtunded, stuporous, seizures, blurred vision, transient blindness
    • Primary Hypertension Nursing DiagnosesAssess: Cardiovascular status; adherence to therapy; family interaction; risk factor modification?Nsg Action: Supportive & reality-based; Administer meds; referrals; diagnostic preps; ask questions; supportive care during hospitalization for acute crisisPt/Family Education: Medications; risk factor modification; Community support
    • HypertensionDynamics of Treatment
    • Primary Hypertension Case Study