Diagnosis requires the measurement of blood pressure on at least two separate occasions averaging two readings at least 2 minutes apart, with the individual seated, the arm supported at heart level, after 5 minutes rest, with no smoking or caffeine intake in the past 30 minutes.
Arteriosclerosis and hypertension.
A break in the vessel wall, usually caused by trauma.
Inflammation (with the production of toxic oxygen radicals) and changes in cytokines, such as TGF-β.
Likely because of improvements in risk factor management.
Variable symptoms and signs related to the size of the aneurysm and the potential for rupture and hemorrhage.
Emergent evaluation and surgical intervention.
Excess aldosterone promotes sodium retention and initiation of the hemodynamics of early hypertension.
It is a mineralocorticoid that causes salt and water retention.
Embolism causes ischemia or infarction in tissues distal to the obstruction.
Sustained hypertension can cause central nervous system dysfunction, impaired vision, impaired mobility, vascular occlusion, or edema.
Because of constant stress on the vessel wall and the absence of penetrating vasa vasorum in the media layer.
It becomes more fibrotic but continues to bulge with each systole, acting as a 'reservoir' for some of the stroke volume.
Greater than 50%.
Disturbances in filtration and reabsorption of serum sodium, potassium, and calcium initiate the hemodynamics of early hypertension.
Higher systemic blood pressure is required to maintain adequate cerebral perfusion.
Renal complications are parenchymal damage, nephrosclerosis, renal arteriosclerosis, and renal insufficiency or failure.
If elevated blood pressure is not detected and treated, it becomes established and may begin to accelerate its effect on tissues when the individual is 30 to 50 years of age.
A greater emphasis on managing the RAAS in hypertension as a first-line intervention.
Endocrine disorders, metabolic disorders, or diseases of the central or peripheral nervous system.
No curative treatment is available.
Thrombi form on heart valves altered by calcification or bacterial vegetation.
Collagen disorders such as Marfan syndrome.
Some individuals benefit from 24-hour ambulatory blood pressure monitoring because of better correlation with end-organ damage and the ability to screen out 'white coat hypertension' and 'masked hypertension'.
Treatment begins with reducing or eliminating risk factors.
Dysrhythmias, heart failure, and embolism of clots to the brain or other vital organs.
A devastating complication that can involve any part of the aorta and can disrupt flow through arterial branches, creating a surgical emergency.
Mucopolysaccharide deposits in vascular tissue increase resistance.
Possibly caused by sodium retention, plasma retention, weight gain, changes in levels and actions of renin, angiotensin, and aldosterone.
Myocardial hypertrophy in response to hypertension is mediated by several neurohormonal substances, including the SNS and angiotensin II.
Changes in the vascular beds can be estimated by viewing the arterioles of the retina.
Potential pathologic effects on the brain include transient ischemic attacks, cerebral thrombosis, aneurysm, hemorrhage, and acute brain infarction.
An exercise program that promotes endurance and relaxation.
A decrease in systolic and diastolic arterial blood pressure on standing.
Multiple system atrophy (MSA) and Parkinson disease.
A localized dilation or outpouching of a vessel wall or cardiac chamber.
In septic shock, systemic inflammation activates the intrinsic and extrinsic pathways of coagulation, resulting in microvascular thrombosis throughout the systemic arterial circulation.
Gene polymorphisms for the production of growth factors and myosin.
Evaluation should include a complete medical history, assessment of lifestyle and other risk factors for hypertension and cardiovascular disease, and evidence of possible secondary causes of hypertension.
5.2%.
Flow to an extremity, causing symptoms of ischemia.
Persistent chronic hypertension and inflammation.
Glucocorticoids facilitate sodium and water retention, initiating the hemodynamics of early hypertension.
Chronic hypertension has been linked to cognitive decline with aging.
If blood pressure is not reduced, cerebral edema and cerebral dysfunction increase until death occurs.
Potential pathologic effects on the heart include left ventricular hypertrophy, myocardial ischemia, and left heart failure.
Relaxation reduces levels of circulating catecholamines, which reduces vascular tone and blood pressure.
Compensatory changes mediated through stretch receptors (baroreceptors) in the carotid sinus and the aortic arch.
As a weakening of the vessel wall, most being fusiform and circumferential.
Pharmacologic treatment of arterial thrombi involves the administration of heparin, warfarin derivatives, thrombin inhibitors, or thrombolytics.
Cholesterol embolization syndrome or atheroembolism is the phenomenon where embolism occurs due to rupture or mechanical disruption of an atherosclerotic plaque.
The great intra-abdominal pressures generated during labor and delivery may force amniotic fluid into the mother’s bloodstream through the highly vascular uterine wall.
Treatment consists of prompt immobilization of fractures and supportive measures including supplemental oxygen, steroids, and glucose.
They are related to frostbite, trauma, or the use of sympathomimetic drugs.
It tends to affect young women.
Traumatic injury to the chest or abdomen.
It is especially recommended for individuals with drug resistance, hypotensive symptoms with medications, episodic hypertension, and autonomic dysfunction.
Lifestyle modification can prevent hypertension from developing in those individuals who fall into the prehypertension category, may control the blood pressure in stage I hypertension, and can enhance the effects of drug treatment for those with more significant blood pressure elevation.
The pressure of a thoracic aneurysm on surrounding organs.
When there is trauma to the aorta or tissue ischemia and necrosis at the edge of an atherosclerotic plaque that weakens the intima.
Increased inotropic effect on the heart elevates systolic pressure; diastolic pressure decreases due to decreased peripheral resistance.
Same as for Cushing syndrome, facilitating sodium and water retention.
Complications specific to the retina include retinal vascular sclerosis, exudation, and hemorrhage.
Capillary permeability is increased by high hydrostatic pressures in the capillaries, and vascular fluid exudes into the interstitial space.
To eliminate the vasoconstrictor effects of nicotine.
Hypotension with no known initial cause.
An extravascular hematoma that communicates with the intravascular space.
A balloon-tipped catheter can be used to remove or compress an arterial thrombus.
The immediate threat to life is the occlusion of a coronary artery causing an MI or the occlusion of a cerebral artery causing a stroke.
Amniotic fluid displaces blood, reducing oxygen, nutrient, and waste exchange, and introduces antigens, cells, and protein aggregates that trigger inflammation, coagulation, and the immune response within the bloodstream.
Platelets adhere to fat globules until the conglomerate is large enough to lodge in a capillary bed.
Fusiform circumferential and fusiform saccular aneurysms.
Optional tests include urinary albumin excretion or albumin/creatinine ratio.
Infarct expansion, a weak and thin layer of necrotic muscle, and fibrous tissue that bulges with each systole.
When aortic aneurysms reach 5 cm in diameter.
Impaired blood flow and renal ischemia invoke the compensatory renin-angiotensin-aldosterone mechanism to raise renal perfusion pressure.
Loss of elasticity in vessel walls results in increased peripheral resistance.
Hypertension may develop in an individual who routinely takes a monoamine oxidase (MAO) inhibitor with ingestion of a food containing tyramine, such as aged cheese.
ACE inhibitors, ARBs, or aldosterone antagonists.
Secondary to a specific disease or idiopathic (primary).
Up to 18%.
Conditions such as intimal irritation and roughening, inflammation, traumatic injury, infection, and low blood pressures or obstructions that cause blood stasis and pooling within the vessels can activate the coagulation or clotting cascade.
Arterial emboli most commonly originate in the left heart and are associated with thrombi after MI, valvular disease, left heart failure, endocarditis, and dysrhythmias.
More than half of arterial thromboemboli lodge in the lower extremities, specifically in the femoral and popliteal arteries.
Supportive measures may include dialysis.
Infections such as syphilis.
No, a single elevated blood pressure reading does not mean a person has hypertension.
Treatment of primary hypertension depends on its severity.
Optimize dosages or add additional drugs until goal BP is achieved, and consider consultation with a hypertension specialist.
Aneurysm repair even in those individuals with acute symptoms or complications.
Disturbance in filtration and/or reabsorption of serum sodium.
They interface with neural control of blood pressure, initiating increased systemic blood pressure.
Microalbuminuria (small amounts of protein in the urine) is an early sign of impending renal dysfunction and significantly increased risk for cardiovascular events.
The complications of hypertension begin to appear during the fourth, fifth, and sixth decades of life.
Potential pathologic effects on the aorta include aneurysms and acute aortic syndromes.
Combinations of thiazide diuretics and other antihypertensives, such as beta-blockers and ACE inhibitors.
Cardiovascular autonomic neuropathy.
Impotence and bowel and bladder dysfunction.
When the underlying disorder is corrected.
Widespread arterial thrombus formation can occur in shock, particularly shock resulting from septicemia.
Embolism to a central organ causes organ dysfunction and pain.
Heart failure is associated with an increased risk of thrombotic complications, although the mechanism for this increased risk is unclear.
Aggregates of bacteria can cause bacterial embolism.
Because plaque formation erodes the vessel wall.
Individuals who have elevated blood pressure are assumed to have primary hypertension unless their history, physical examination, or initial diagnostic screening indicates secondary hypertension.
Two-drug combination for most (usually thiazide-type diuretic and ACE inhibitor or ARB or beta-blocker or CCB).
Approaches 20%.
Elevated blood renin levels invoke elevations in angiotensin and aldosterone, causing blood pressure to rise.
Pathogenesis unclear.
Vascular complications include the formation, dissection, and rupture of aneurysms, intermittent claudication, and gangrene resulting from vessel occlusion.
The likelihood of developing primary hypertension increases with age, over and above the natural rise in blood pressure associated with aging.
Conditions such as heart failure, chronic kidney disease, postmyocardial infarction, or recurrent stroke.
Postural reflexes are slowed as part of the aging process.
Men more often than women, usually between the ages of 40 and 70 years.
Pulmonary emboli originate in the venous circulation, mostly from the deep veins of the legs, or in the right heart.
Mitral or aortic valvular disease, especially that associated with abnormal heart rhythms (atrial fibrillation and flutter), causes thrombus formation on roughened vascular surfaces and in atrial blood.
Steroid administration may decrease the inflammation that occurs with vascular occlusion.
Inflammatory lesions are accompanied by thrombi and sometimes by vasospasm of arterial segments.
Pressure-tension and wall thickness relations.
Physical examination should include examination of the optic fundi, calculation of body mass index, auscultation for carotid, abdominal, and femoral bruits, examination of the heart and lungs, palpation of the abdomen, assessment of lower extremity pulses and edema, and neurologic examination.
The usual dietary recommendations are to restrict sodium intake to 2.4 g/day, to increase potassium intake, to restrict saturated fat intake, and to adjust calorie intake as required to maintain optimum weight.
By ultrasonography, CT, MRI, or angiography.
Excess production of adrenocortical hormones promotes sodium and water retention.
Cardiovascular complications include left ventricular hypertrophy, angina pectoris, congestive heart failure (left heart failure), CAD, MI, and sudden death.
Organ damage resulting from malignant hypertension can cause encephalopathy, papilledema, cardiac failure, uremia, retinopathy, and cerebrovascular accident.
Lipid disorders and glucose intolerance.
Altered body chemistry, drug action, prolonged immobility, starvation, physical exhaustion, volume depletion, and venous pooling.
Anatomic changes of an artery, such as an aneurysm, can stimulate thrombus formation, particularly if the change results in pooling of arterial blood.
When an embolus reaches a vessel through which it cannot fit, it lodges in a systemic or pulmonary vessel, causing obstruction.
The most common source of arterial thromboemboli to the systemic circulation is the heart.
Trauma to the long bones is associated with fat embolism.
It usually is removed surgically.
The chief symptoms are pain and tenderness of the affected part.
Routine diagnostic tests include hematocrit, urinalysis, biochemical blood profile (fasting glucose, sodium, potassium, calcium, creatinine, total cholesterol, high-density cholesterol, triglycerides), and an electrocardiogram (ECG).
The Dietary Approaches to Stop Hypertension (DASH) diet is recommended.
Smoking cessation, reducing blood pressure and blood volume, and β-adrenergic blockage.
Excess catecholamines raise vascular tone and increase peripheral resistance.
The early stages of hypertension have no clinical manifestations other than elevated blood pressure.
To reduce the risk of end-organ damage and prevent major diseases such as myocardial ischemia and stroke.
A prompt increase in heart rate and constriction of the systemic arterioles, maintaining stable blood pressure.
24-hour blood pressure monitoring.
A leak between a vascular graft and a natural artery.
Embolism is the obstruction of a vessel by an embolus, which is a bolus of matter circulating in the bloodstream.
Infarction and subsequent necrosis of a central organ are life-threatening because of organ dysfunction and the risk of sepsis.
The capillary beds of the lungs and kidneys are usually affected by amniotic fluid emboli.
No, isolated bacteria in the bloodstream do not cause embolism.
Inflammation in the pulmonary bed can cause acute respiratory distress syndrome (ARDS).
If vasospasm persists, sympathectomy may be performed.
Chronic hypertension.
Dissecting aneurysm.
Loss of medial elastic lamellae and thinning of the tunica media.
Formation of a ventricular wall aneurysm.
To maintain a low blood volume and low blood pressure to decrease mechanical forces thought to contribute to vessel wall dilation.
Disturbances in filtration and reabsorption of serum sodium, potassium, and calcium.
Excess catecholamines raise vascular tone and increase peripheral resistance.
The increased size of the heart muscle increases demand for oxygen delivery over time, contractility of the heart is impaired, and the individual is at increased risk for systolic heart failure.
Although hypertension is usually thought to be an adult health problem, it is important to remember that hypertension does occur in children and is being diagnosed with increasing frequency.
Potential pathologic effects on the coronary arteries include myocardial ischemia, myocardial infarction, and sudden death.
Diuretics and beta-blockers.
Falls, associated injuries, and an increased risk for cardiovascular events.
The activation of the coagulation cascade in the arteries is usually caused by roughening of the tunica intima by atherosclerosis.
Valvular thrombi are most commonly associated with inflammation of the endocardium (endocarditis) and rheumatic heart disease.
A limb that is ischemic because of arterial occlusion is characterized by an almost waxy whiteness of the skin and numbness and pain resulting from neural ischemia.
The first mechanism is defective fat metabolism causing globules of fat to form in the blood, and the second is the release of fat globules from fatty bone marrow exposed by fracture.
It is an inflammatory disease of the peripheral arteries.
Ambulatory measurement detects those who fail to have a nocturnal decrease in blood pressure and who may be at higher cardiovascular risk.
12.5%.
When they rupture, becoming painful.
Dissection of the layers of the arterial wall.
Calcium ion directly affects vascular tonicity; elevated serum calcium levels increase vascular tone and peripheral resistance.
Potential pathologic effects on the eyes include retinal vascular sclerosis, exudation, and hemorrhage.
Physical training increases stroke volume, which lowers heart rate and systolic blood pressure.
A systolic blood pressure decrease of at least 20 mmHg or a diastolic blood pressure decrease of at least 10 mmHg within 3 minutes of standing up.
Supine hypertension, altered drug sensitivity, hyperresponsiveness of blood pressure to hypo/hyperventilation, sleep apnea, and other neurologic disturbances.
All three layers of the arterial wall.
The diagnosis of arterial thrombi is usually accomplished through the use of Doppler ultrasonography and angiography.
Embolism in the coronary, cerebral, and peripheral arterial systems may occur as a result of rupture or mechanical disruption of an atherosclerotic plaque.
Treatment for air embolism is supportive, including bed rest and supplemental oxygen, once the connection between the source of air and the vascular system is eliminated.
Clumps of vegetation are dislodged from infected cardiac valves and ejected into the pulmonary or systemic circulation.
These small particles initiate the coagulation cascade.
In the thoracic or abdominal aorta.
Thiazide-type diuretics for most, may consider ACE inhibitor, ARB, beta-blocker, CCB, or combination.
For those aneurysms that are dilating rapidly.
Decreased blood flow in distal areas initiates maximum peripheral resistance as an autoregulatory effort to adjust perfusion pressure.
They raise vascular tone and increase vascular resistance.
Hypertrophy is characterized by changes in the myocyte proteins, apoptosis of myocytes, and deposition of collagen in heart muscle, causing it to become thickened, scarred, and less able to relax during diastole leading to diastolic heart failure.
Malignant hypertension is rapidly progressive hypertension in which diastolic pressure is usually greater than 140 mmHg and can cause encephalopathy.
Hypertension is called a 'silent' disease because the lack of signs and symptoms means the individual is unlikely to seek health care.
Thiazide diuretics and beta-blockers.
They are not effective in maintaining a stable blood pressure.
Basically spherical.
An embolus may consist of a dislodged thrombus, an air bubble, an aggregate of amniotic fluid, an aggregate of fat, bacteria, or cancer cells, or a foreign substance.
Thromboembolism is a vascular obstruction resulting from a dislodged thrombus.
Rubor is redness of the skin caused by dilated capillaries under the skin.
1.3%.
Where the aneurysm is located.
Acute aortic syndromes that include aortic dissection, hemorrhage into the vessel wall, or vessel rupture.
Excess human growth hormone causes increased peripheral resistance.
Acute stress precipitates the release of catecholamines and glucocorticoids.
Encephalopathy occurs because high arterial pressure renders the cerebral arterioles incapable of regulating blood flow to the cerebral capillary beds.
The clinical manifestations of chronic hypertension tend to be specific for the organs or tissues affected.
Potential pathologic effects on the kidneys include nephrosclerosis leading to renal failure.
The DASH diet.
Renal denervation.
Dizziness, blurring or loss of vision, and syncope or fainting.
Liberalization of salt intake, raising the head of the bed, thigh-high stockings, volume expansion with mineralocorticoids, and vasoconstrictors such as midodrine.
Renal artery embolism causes abdominal pain and oliguria.
Large amounts of air cannot be dissolved rapidly enough to prevent the displacement of blood in the arterioles and capillary beds, leading to ischemia and necrosis.
A less common cause is the erosion of an artery or vein by bacteria at a source of infection, such as an abscess.
The thromboemboli can occlude a vessel and result in ischemia.
It can be an important clue to finding a previously undiagnosed cancer.
Cerebrovascular complications include transient ischemia, stroke, cerebral thrombosis, aneurysm, and hemorrhage.
Potential pathologic effects on the arterial vessels of the lower extremities include intermittent claudication, arterial thrombosis, and gangrene.
Regular aerobic physical activity.
Arteriolar, venular, or mixed.
Laplace’s law.
The invasion of the tunica intima by an infectious agent roughens the normally smooth lining of the artery, causing platelets to adhere readily.
The two potential threats posed by arterial thrombi to the circulation are that the thrombus may grow large enough to occlude the artery, causing ischemia in tissue supplied by the artery, and the thrombus may dislodge, becoming a thromboembolus that travels through the vascular system until it occludes flow into a distal systemic vascular bed.
Mesenteric artery embolism causes abdominal pain and a paralytic, ischemic bowel.
Air can be introduced into the bloodstream if trauma to the chest causes air from the lungs to enter the vascular space, such as in gunshot wounds and puncture wounds of the thorax.
It has been declining presumably because of a decrease in cigarette smoking in men.
The clinical manifestations are the same, but their causes differ.
Vasospastic attacks are triggered by brief exposure to cold or by emotional stress.
Pulmonary artery embolism causes chest pain and dyspnea.
Room air that enters the circulation through intravenous lines is probably the most common cause of air embolism.
The most common cause of bacterial embolism is subacute bacterial endocarditis.
Small particles such as drug precipitates, small glass shards, or fibers from linen can be introduced.
The pathogenesis is still being explored, with evidence of significant T-cell activation and autoimmunity, as well as a lack of appropriate production of endothelial precursor cells in the bone marrow.
They can eventually occlude and obliterate portions of small and medium-size arteries.
Raynaud phenomenon is secondary to systemic diseases such as collagen vascular disease, chemotherapy, cocaine use, hypothyroidism, pulmonary hypertension, thoracic outlet syndrome, serum sickness, vasculitis, malignancy, or long-term exposure to environmental conditions.
Arterial thromboemboli can also lodge in the coronary arteries and the cerebral vasculature.
Treatment includes bed rest, supplemental oxygen, and antibiotics to eradicate the source of infection.
Treatment is aimed at preventing thrombus formation around the particle, dissolution of the particle, and supportive measures to alleviate ischemia.
Cyanosis is caused by blood that remains in the capillaries after its oxygen has diffused into the interstitium.
They are characterized by attacks of vasospasm in the small arteries and arterioles of the fingers and, less commonly, the toes.
Raynaud disease is a primary vasospastic disorder of unknown origin.
Chronic ischemia causes the skin to thin and become shiny and the nails to become thickened and malformed.
Foreign matter can enter the bloodstream during trauma or through an intravenous or intra-arterial line.
The digital, tibial, and plantar arteries of the feet and the digital, palmar, and ulnar arteries of the hands are typically affected.
Newer therapies include immunomodulation, spinal cord stimulation, and bone marrow transplantation.
It is associated with smoking in approximately 95% of cases.
Clinical manifestations are caused by sluggish blood flow.
Platelet activation may play a role in Raynaud disease.
Advanced disease can lead to gangrene, which may require amputation.
Other measures include exercise and dependent positioning to improve circulation, vasodilators to alleviate vasospasm, and antithrombotics to prevent thrombus formation.
They demonstrate endothelial dysfunction with an imbalance in endothelium-derived vasodilators and vasoconstrictors.
The most important part of treatment is cessation of cigarette smoking.
The five primary criteria are: (1) onset before age 50; (2) history of tobacco use; (3) ischemia of the digits; (4) typical arteriographic findings; and (5) exclusion of autoimmune disease, thrombophilia, diabetes, and proximal embolic source.
Genetic predisposition may play a role in its development.
