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80 Cards in this Set

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Cardiac Output X Systemic Vascular Resistance
Arterial BP
Sroke volume X beats per minute
Cardiac Output
Force opposing the movement of blood within the blood vessels.
Systemic vascular resistance
What are the four mechanisms that regulate the BP?
Sympathetic nervous system

Vascular endothelium

Renal system

Endocrine system
norepinephrine released from sympathetic nerve endings - to receptors alpha1, alpha2, beta 1 & beta2
Sympathetic Nervous System
What are five details about the sympathetic nervous system
Reacts within seconds

Increases Heart Rate - chronotropic

Increased cardiac contractility - inotropic

Produces widespread vasoconstriction in peripheral arterioles

Promotes release of renin from the kidney
This interacts with many areas of the brain to maintain BP within normal range under various conditions.
Sympathetic vasomotor center located in the medulla
What are two examples of the sympathetic vasomotor center function?
Exercise - Changes to meet oxygen demand

Postural changes - Peripheral vasoconstriction
Specialized nerve cells, a part of the SNS, in the carotid arteries and the aortic arch.
Baroreceptors
When the baroreceptors experience a BP change, what SNS changes occur?
Inhibits SNS – peripheral vessel dilation. Decreased heart rate, and decreased contractility of the heart + increased parasympathetic activity (vagus nerve) decreased heart rate
When the baroreceptors experience a decrease in BP what SNS changes occur?
Decrease: Activates SNS – peripheral vessel constriction, increased heart rate, and increased contractility of the heart
This may contribute to atherosclerosis & primary hypertension?
Endothelial dysfunction
This is a single cell layer that lines the blood vessels?
Vascular endothelium
The vascular endothelium produces three vasoactive substances, what are they?
EDRF Endothelium-derived relaxing factor

Vasodilation - prostacyclin

Endothelin (ET) potent vasoconstrictor
Helps maintain low arterial tone at rest
Inhibits growth of the smooth muscle layer
Inhibits platelet aggregation
EDRF Endothelium-derive relaxing factor
A prostaglandin produced in the walls of blood vessels; it acts as a vasodilator and inhibits the aggregation of platelets.
Vasodilation – prostacyclin
What three aspects of the renal system help control BP?
Control Na+ excretion & extracellular fluid volume

Renin-angiotensin-aldosterone

Renal Medulla
How does the Renin-angiotensin-aldosterone system work?
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
This secretes Prostaglandins - having a vasodilator effect
Renal Medulla
The endocrine stimulates the SNS in what three ways?
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
This releases Aldosterone – stimulates kidneys to retain Na+
Adrenal Cortex
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
Specific cause of Secondary hypertension can be identified 5+% of adult hypertension, what are some of these?
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
Narrowing or constriction of the lumen of the aorta ~ 7% of patients with congenital heart disease.
2x as common in males

Symptoms:
HA
Epistaxis
Cold extremities
Claudication with exercise
Coarctation of the Aorta
What are the physical findings for coarctation of the aorta?
Pulse lag in lower extremities

Systolic BP 20 mmHg or more higher in the upper than in the lower extremities

Blowing systolic murmur in the left axilla
This is the most common cause of secondary HTN.

May result from:
Diabetic and inflammatory glomerular disease
Tubular interstitial disease
Polycystic kidneys
Renal parenchymal disease
Abrupt onset of HTN before age 50
Consider?
Fibromuscular Dysplasia
Abrupt onset of HTN at or after the age of 50?
Suggestive of atherosclerotic renal artery stenosis
Tumors that arise from the adrenal medulla
Rare – 2/million population
Rule of 10’s:
10% cases occur in children
10% cases involve both adrenal glands
10% cases have metastatic disease at time of diagnosis
Pheochromocytoma
How do pheochromocytomas cause HTN?
They produce, store and secrete the catecholamines norepinephrine and epinephrine.
Syndrome due to supraphysiologic doses of corticosteroids

Disease due to ACTH hypersecretion by the pituitary secondary to a pituitary adenoma

5-10x more common in women
Cushing Syndrome aka Cushing Disease (Hypercortisolism)
What are the signs and symptoms of Cushing Syndrome?
Obesity or weight gain
Truncal Obesity
Thin skin
Moon face
HTN
Purple skin striae
Hirsuitism
Abnormal glucose tolerance
menstrual irregularities
Impotence
Acne
Bruising
Mental changes
Osteoporosis
Edema of the lower extremities
How do you test for Cushings?
Dexamethasone suppression testing
Salivary cortisol followed by dexamethasone orally with sequential serum cortisol levels

If results are abnormal:
24-hour urine collection for free cortisol and creatinine

ACTH level (less that 20 picograms/mL indicate probable adrenal tumor
Excessive and inappropriate aldosterone production.

Generally caused by a unilateral adenoma
2x greater incidence in women

Occurs between 30-50 yrs of age

In pts. with HTN = ~1%

Prevalence as high as 5%
Primary Aldosteronism
Signs and symptoms of primary aldosteronism?
Hypokalemia = muscle weakness and fatigue

Headaches

Polyuria and polydipsia
What can be expected in the Physical Exam, EKG and X-Ray in primary aldosteronism?
Diastolic hypertension (sometimes very severe) without edema
LVH
U waves
Cardiac arrhythmias
Premature contractions
Proteinuria (50% of those affected)
15% Renal failure
Hyposecretion of renin (low plasma renin activity levels)
Adenoma identified by abd. CT scan
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 (Essential) Hypertension:
What is the pathophysiology of primary hypertension?
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
What are the signs of severe HTN?
fatigue, reduced activity tolerance, dyspnea, dizziness, palpitations, angina
Grade I retinopathy shows?
Narrowing of arterioles
Grade II retinopathy shows?
AV nipping
Flame hemorrhages
Grade III retinopathy shows?
Extensive hemorrhages
Retinal exudates
Cotton wool patches
Grade IV retinopathy shows?
Exaggerated changes of grade III
Disk edema (not papilledema)
In what patients is SBP a more important than DBP as a CVD risk factor.
Patients over age 50
This drug should be initial drug therapy for most, either alone or combined with other drug classes.
Thiazide diuretics
BP Measurement Techniques:

In Office?
Two readings, 5 minutes apart, sitting in chair. Confirm elevated reading in contralateral arm.
BP Measurement Techniques:

Ambulatory BP Monitoring
Indicated for evaluation of “white-coat” HTN. Absence of 10–20% BP decrease during sleep may indicate increased CVD risk.
BP Measurement Techniques:

Self Measurement
Provides information on response to therapy. May help improve adherence to therapy and evaluate “white-coat” HTN.
Evaluation of patients with documented HTN has three objectives:
Assess lifestyle and identify other CV risk factors or concomitant disorders that affects prognosis and guides treatment.

Reveal identifiable causes of high BP.

Assess the presence or absence of target organ damage and CVD.
What are the examples of target organ damage caused by HTN and CVD?
Left Ventricular Hypertrophy
Angina or prior myocardial infarction
Prior coronary revascularization
Heart Failure
Stroke or transient ischemic attack
Chronic kidney disease
Peripheral arterial disease
Retinopathy
What are the tests that can be used to diagnose and TX HTN and CVD?
Electrocardiogram
Urinalysis
Blood glucose, and hematocrit
Serum potassium, creatinine, or the corresponding estimated GFR, and calcium
Lipid profile, after 9- to 12-hour fast, that includes high-density and low-density lipoprotein cholesterol, and triglycerides
Measurement of urinary albumin excretion or albumin/creatinine ratio
Stage one hypertension?
(SBP 140–159 or DBP 90–99 mmHg) Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination.
Stage two hypertension?
(SBP >160 or DBP >100 mmHg) 2-drug combination for most (usually thiazide-type diuretic and ACEI, or ARB, or BB, or CCB)
What should be measured 1-2 times a year with HTN tx?
Serum potassium and creatinine monitored 1–2 times per year.
What are the HTN Tx options with heart failure?
THIAZ, BB, ACEI, ARB, ALDO ANT
What are the HTN Tx options with post MI?
BB, ACEI, ALDO ANT
What are the HTN Tx options with high CAD risks?
THIAZ, BB, ACE, CCB
What are the HTN Tx options with Diabetes?
THIAZ, BB, ACE, ARB, CCB
What are the HTN Tx options with kidney disease?
ACEI, ARB
What are the HTN Tx options with recurrent stroke prevention?
THIAZ, ACEI
African Americans demonstrate somewhat reduced BP responses to
monotherapy with BBs, ACEIs, or ARBs compared to diuretics or CCBs.
is an independent risk factor that increases the risk of CVD.
LVH
Regression of LVH occurs with aggressive BP management including what things?
weight loss, sodium restriction, and treatment with all classes of drugs except the direct vasodilators hydralazine and minoxidil.
This is equivalent in risk to ischemic heart disease.

Any class of drugs can be used in most of these patients.

Other risk factors should be managed aggressively.

Aspirin should be used.
Peripheral Artery Disease
Decrease in standing SBP >10 mmHg, when associated with dizziness/fainting, more frequent in older SBP patients with diabetes, taking diuretics, venodilators, and some psychotropic drugs.

BP in these individuals should be monitored in the upright position.

Avoid volume depletion and excessively rapid dose titration of drugs.
Postural Hypotension
What should be used in pregnancy to tx HTN?
Methyldopa, BBs, and vasodilators, preferred for the safety of the fetus.
What is contraindicated in the Tx of HTN in pregnant patients?
ACEI and ARBs contraindicated in pregnancy
HTN defined as BP—95th percentile or greater, adjusted for age, height, and gender.

Use lifestyle interventions first, then drug therapy for higher levels of BP or if insufficient response to lifestyle modifications.
HTN in children and adolescents
This is not a reason to restrict physical activity in children.
Uncomplicated HTN
useful in slowing demineralization in osteoporosis.
Thiazide-type diuretics
useful in the treatment of atrial tachyarrhythmias/fibrillation, migraine, thyrotoxicosis (short-term), essential tremor, or perioperative HTN.
Beta Blockers
useful in Raynaud’s syndrome and certain arrhythmias
Calcium Channel Blockers
useful in prostatism.
Alpha Blockers
should be used cautiously in gout or a history of significant hyponatremia.
Thiazide diuretics
should be generally avoided in patients with asthma, reactive airways disease, or second- or third-degree heart block.
Beta Blockers
are contraindicated in pregnant women or those likely to become pregnant.
ACEIs and ARBs
should not be used in individuals with a history of angioedema.
ACEI
can cause hyperkalemia.
Aldosterone antagonists and potassium-sparing diuretics
Causes of resistant HTN?
Improper BP measurement

Excess sodium intake

Inadequate diuretic therapy

Medication
Inadequate doses
Drug actions and interactions (e.g., nonsteroidal anti-inflammatory drugs (NSAIDs), illicit drugs, sympathomimetics, oral contraceptives)
Over-the-counter (OTC) drugs and herbal supplements

Excess alcohol intake

Identifiable causes of HTN