Download primary function of cardiac output and systemic vascular resistance

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
Hypertension
Arterial BP = Cardiac Output (CO) x Systemic
vascular resistance (SVR)
Cardiac Output = stroke volume x beats per min
Systemic vascular resistance = force opposing the
movement of blood within the blood vessels
What is the effect on BP if SVR increased and CO
remains constant?
Hypertension
Mechanisms 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
Hypertension
SNS 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
Hypertension
Renin-Angiotensin
Hypertension
Renin-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
Hypertension
Aldosterone 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 Manifestation
Dx is made after multiple readings over several weeks
NIH/Joint Committee Definition:
Category
Optimal
Normal
High Normal
Systolic
<110
<120
130-139
and
and
or
Stage 1
Stage 2
Stage 3
140-159
160-179
=>180
or
or
or
Diastolic
< 80
<85
85-89
90-99
100-109
=> 110
Primary Hypertension
Risk Factors
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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 Hypertension
Medical Management
Risk Stratification
Level of BP
Presence of Target Organ Disease
Other Risk Factors
Hypertension
Medical Management
Risk Stratification
Primary Hypertension
Medical Management
 Lifestyle modification
 Nutritional therapy
 Alcohol consumption
 Physical activity
 Tobacco avoidance
 Stress management
 Drug Therapy
Hypertension
Nutrition
Hypertension
Risk Factor Modification
Primary Hypertension
Medical Management
Stepped Approach
Lifestyle modification
Not at Goal BP
Drug Therapy
Not at Goal BP
Substitute med / add a 2nd med/ increase dose
Not at Goal BP
Continue 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
Hypertension
Medication - Diuretics
Hypertension
Medication – Beta-blocking Agents
Hypertension
Medication
Calcium Channel Blockers
Hypertension
Medication
Alpha Agonists & Vasodilators
Hypertension
Antihypertensive Drug Therapy
Primary Hypertension
Lack 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, preeclampsia, 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 Diagnoses
Assess: 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 crisis
Pt/Family Education: Medications; risk factor
modification; Community support
Hypertension
Dynamics of Treatment
Primary Hypertension
Case Study