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80 Cards in this Set
- Front
- Back
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Cardiac Output X Systemic Vascular Resistance
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Arterial BP
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Sroke volume X beats per minute
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Cardiac Output
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Force opposing the movement of blood within the blood vessels.
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Systemic vascular resistance
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What are the four mechanisms that regulate the BP?
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Sympathetic nervous system
Vascular endothelium Renal system Endocrine system |
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norepinephrine released from sympathetic nerve endings - to receptors alpha1, alpha2, beta 1 & beta2
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Sympathetic Nervous System
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What are five details about the sympathetic nervous system
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Reacts within seconds
Increases Heart Rate - chronotropic Increased cardiac contractility - inotropic Produces widespread vasoconstriction in peripheral arterioles Promotes release of renin from the kidney |
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This interacts with many areas of the brain to maintain BP within normal range under various conditions.
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Sympathetic vasomotor center located in the medulla
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What are two examples of the sympathetic vasomotor center function?
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Exercise - Changes to meet oxygen demand
Postural changes - Peripheral vasoconstriction |
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Specialized nerve cells, a part of the SNS, in the carotid arteries and the aortic arch.
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Baroreceptors
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When the baroreceptors experience a BP change, what SNS changes occur?
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Inhibits SNS – peripheral vessel dilation. Decreased heart rate, and decreased contractility of the heart + increased parasympathetic activity (vagus nerve) decreased heart rate
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When the baroreceptors experience a decrease in BP what SNS changes occur?
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Decrease: Activates SNS – peripheral vessel constriction, increased heart rate, and increased contractility of the heart
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This may contribute to atherosclerosis & primary hypertension?
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Endothelial dysfunction
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This is a single cell layer that lines the blood vessels?
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Vascular endothelium
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The vascular endothelium produces three vasoactive substances, what are they?
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EDRF Endothelium-derived relaxing factor
Vasodilation - prostacyclin Endothelin (ET) potent vasoconstrictor |
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Helps maintain low arterial tone at rest
Inhibits growth of the smooth muscle layer Inhibits platelet aggregation |
EDRF Endothelium-derive relaxing factor
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A prostaglandin produced in the walls of blood vessels; it acts as a vasodilator and inhibits the aggregation of platelets.
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Vasodilation – prostacyclin
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What three aspects of the renal system help control BP?
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Control Na+ excretion & extracellular fluid volume
Renin-angiotensin-aldosterone Renal Medulla |
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How does the Renin-angiotensin-aldosterone system work?
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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 |
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This secretes Prostaglandins - having a vasodilator effect
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Renal Medulla
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The endocrine stimulates the SNS in what three ways?
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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 |
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This releases Aldosterone – stimulates kidneys to retain Na+
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Adrenal Cortex
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Increased Na+ stimulates?
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posterior pituitary – ADH – reabsorbs ECF/water
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Hypertension Aldosterone Mechanism:
Increased Aldosterone = |
Increases sodium reabsorption =
Increases water reabsorption = Increases blood volume = Increases cardiac output |
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Specific cause of Secondary hypertension can be identified 5+% of adult hypertension, what are some of these?
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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 |
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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
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What are the physical findings for coarctation of the aorta?
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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 |
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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
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Abrupt onset of HTN before age 50
Consider? |
Fibromuscular Dysplasia
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Abrupt onset of HTN at or after the age of 50?
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Suggestive of atherosclerotic renal artery stenosis
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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
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How do pheochromocytomas cause HTN?
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They produce, store and secrete the catecholamines norepinephrine and epinephrine.
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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)
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What are the signs and symptoms of Cushing Syndrome?
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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 |
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How do you test for Cushings?
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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 |
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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
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Signs and symptoms of primary aldosteronism?
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Hypokalemia = muscle weakness and fatigue
Headaches Polyuria and polydipsia |
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What can be expected in the Physical Exam, EKG and X-Ray in primary aldosteronism?
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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 |
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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:
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What is the pathophysiology of primary hypertension?
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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 |
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What are the signs of severe HTN?
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fatigue, reduced activity tolerance, dyspnea, dizziness, palpitations, angina
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Grade I retinopathy shows?
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Narrowing of arterioles
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Grade II retinopathy shows?
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AV nipping
Flame hemorrhages |
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Grade III retinopathy shows?
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Extensive hemorrhages
Retinal exudates Cotton wool patches |
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Grade IV retinopathy shows?
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Exaggerated changes of grade III
Disk edema (not papilledema) |
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In what patients is SBP a more important than DBP as a CVD risk factor.
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Patients over age 50
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This drug should be initial drug therapy for most, either alone or combined with other drug classes.
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Thiazide diuretics
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BP Measurement Techniques:
In Office? |
Two readings, 5 minutes apart, sitting in chair. Confirm elevated reading in contralateral arm.
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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.
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BP Measurement Techniques:
Self Measurement |
Provides information on response to therapy. May help improve adherence to therapy and evaluate “white-coat” HTN.
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Evaluation of patients with documented HTN has three objectives:
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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. |
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What are the examples of target organ damage caused by HTN and CVD?
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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 |
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What are the tests that can be used to diagnose and TX HTN and CVD?
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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 |
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Stage one hypertension?
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(SBP 140–159 or DBP 90–99 mmHg) Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination.
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Stage two hypertension?
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(SBP >160 or DBP >100 mmHg) 2-drug combination for most (usually thiazide-type diuretic and ACEI, or ARB, or BB, or CCB)
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What should be measured 1-2 times a year with HTN tx?
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Serum potassium and creatinine monitored 1–2 times per year.
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What are the HTN Tx options with heart failure?
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THIAZ, BB, ACEI, ARB, ALDO ANT
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What are the HTN Tx options with post MI?
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BB, ACEI, ALDO ANT
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What are the HTN Tx options with high CAD risks?
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THIAZ, BB, ACE, CCB
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What are the HTN Tx options with Diabetes?
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THIAZ, BB, ACE, ARB, CCB
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What are the HTN Tx options with kidney disease?
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ACEI, ARB
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What are the HTN Tx options with recurrent stroke prevention?
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THIAZ, ACEI
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African Americans demonstrate somewhat reduced BP responses to
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monotherapy with BBs, ACEIs, or ARBs compared to diuretics or CCBs.
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is an independent risk factor that increases the risk of CVD.
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LVH
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Regression of LVH occurs with aggressive BP management including what things?
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weight loss, sodium restriction, and treatment with all classes of drugs except the direct vasodilators hydralazine and minoxidil.
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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
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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
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What should be used in pregnancy to tx HTN?
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Methyldopa, BBs, and vasodilators, preferred for the safety of the fetus.
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What is contraindicated in the Tx of HTN in pregnant patients?
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ACEI and ARBs contraindicated in pregnancy
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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
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This is not a reason to restrict physical activity in children.
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Uncomplicated HTN
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useful in slowing demineralization in osteoporosis.
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Thiazide-type diuretics
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useful in the treatment of atrial tachyarrhythmias/fibrillation, migraine, thyrotoxicosis (short-term), essential tremor, or perioperative HTN.
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Beta Blockers
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useful in Raynaud’s syndrome and certain arrhythmias
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Calcium Channel Blockers
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useful in prostatism.
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Alpha Blockers
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should be used cautiously in gout or a history of significant hyponatremia.
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Thiazide diuretics
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should be generally avoided in patients with asthma, reactive airways disease, or second- or third-degree heart block.
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Beta Blockers
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are contraindicated in pregnant women or those likely to become pregnant.
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ACEIs and ARBs
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should not be used in individuals with a history of angioedema.
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ACEI
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can cause hyperkalemia.
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Aldosterone antagonists and potassium-sparing diuretics
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Causes of resistant HTN?
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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 |
