Transcript diseases of the veins

ALTERATIONS OF
CARDIOVASCULAR
FUNCTION
EUGENE PARDI, DO
MARICOPA COMMUNITY COLLEGES
ESTRELLA MOUNTAIN COMMUNITY
COLLEGE
DISEASES OF THE VEINS:
VARICOSE VEINS & CHRONIC VENOUS
INSUFFICIENCY
▪ VARICOSE VEIN: a vein in which blood has
pooled, producing distended, tortuous, and
palpable vessels.
▪ Caused by:
▪ Trauma to the saphenous veins that
damages one or more valves.
▪ Gradual venous distention caused by the
action of gravity on blood in the legs.
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DISEASES OF THE VEINS:
VARICOSE VEINS & CHRONIC VENOUS
INSUFFICIENCY
▪ If a valve is damaged, a section of the vein is subjected
to the pressure of a larger volume of blood under the
influence of gravity.
▪ The vein swells as it becomes engorged with blood.
▪ Surrounding tissue becomes edematous as increased
hydrostatic pressure pushes plasma through the
stretched vessel wall.
▪ Venous distention develops over time in individuals who
stand for long periods, wear constricting garments, or
cross the legs at the knees.
▪ Diminishes the action of the muscle pump.
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DISEASES OF THE VEINS:
VARICOSE VEINS & CHRONIC VENOUS
INSUFFICIENCY
▪ Risk factors include:
▪ Age
▪ Female gender.
▪ Family history of varicose veins.
▪ Obesity.
▪ Pregnancy.
▪ Deep venous thrombosis.
▪ Previous leg injury
▪ The increased pressure in the vein damages venous
valves, rendering them incompetent and unable to
maintain normal venous pressure.
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DISEASES OF THE VEINS:
VARICOSE VEINS & CHRONIC VENOUS
INSUFFICIENCY
▪ Varicose veins and valvular incompetence can
progress to CHRONIC VENOUS INSUFFICIENCY (CVI).
▪ CVI is inadequate venous return over a long period.
▪ Venous hypertension, circulatory stasis, and tissue
hypoxia cause an inflammatory reaction in vessels
and tissue leading to fibrosclerotic remodeling of
the skin and then to ulceration.
▪ Symptoms: edema of the lower extremities which
may extend to the knee and hyperpigmentation of
the skin of the feet and ankles.
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DISEASES OF THE VEINS:
VARICOSE VEINS & CHRONIC VENOUS
INSUFFICIENCY
▪ Circulation to the extremities can become so
sluggish that the metabolic demands of the cells
are barely met.
▪ Any trauma or pressure can lower the O2 supply
and cause cell death and necrosis (VENOUS
STASIS ULCERS).
▪ Infection can occur due to the sluggish
circulation.
▪Infection following reparative surgery is a
significant risk.
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DISEASES OF THE VEINS:
VARICOSE VEINS & CHRONIC VENOUS
INSUFFICIENCY
▪ Treatment of varicose veins and CVI:
▪ Elevating the legs.
▪ Wearing compression stockings.
▪ Physical exercise.
▪ Sclerotherapy or surgical ligation.
▪ Conservative vein resection.
▪ Vein stripping.
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Before Vein Ablation,
photo courtesy of Dr.
Robert Min
After Vein Ablation,
photo courtesy of Dr.
Robert Min
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Treatment: Support Stockings
Treatment:
Sclerotherapy
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Treatment: Laser Therapy
Sclerotherapy: Before and After
Treatment: Vein Surgery
Treatment: Endovenous Laser
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DISEASES OF THE VEINS:
THROMBUS FORMATION IN VEINS
▪THROMBUS: a blood clot that remains
attached to a vessel wall.
▪THROMBOEMBOLUS: a detached
thrombus.
▪Venous thrombi are more common than
arterial thrombi because flow and
pressure are lower in the veins than in
the arteries.
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DISEASES OF THE VEINS:
THROMBUS FORMATION IN VEINS
▪ DEEP VENOUS THROMBOSIS (DVT): occurs
primarily in the lower extremity.
▪ The TRIAD OF VIRCHOW are three factors that
promote venous thrombosis.
▪Venous stasis (e.g. immobility, age, CHF).
▪Venous endothelial damage (e.g. trauma,
intravenous medications).
▪Hypercoagulable states (e.g. inherited
disorders, malignancy, pregnancy, use of oral
contraceptives, or HRT).
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Contributions from cells, plasma, and
blood flow (Virchow's Triad) regulate
fibrin
formation and therefore, fibrin
network structure and stability.
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DISEASES OF THE VEINS:
THROMBUS FORMATION IN VEINS
▪ Accumulation of clotting factors and platelets
leads to thrombus formation in the vein, often
near a venous valve.
▪ Inflammation promotes further platelet
aggregation, and the thrombus propagates or
grows proximally.
▪ If the vein is deep in the leg, the inflammation
is not accompanied by clinical symptoms or
signs.
▪ If the thrombus creates obstruction to venous
blood flow, edema of the leg may occur.
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DISEASES OF THE VEINS:
THROMBUS FORMATION IN VEINS
▪ THROMBUS FORMATION (CONT’D):
▪ Most thrombi eventually dissolve without
treatment.
▪ Untreated DVT is associated with a high
risk of PULMONARY EMBOLISM.
▪ Persistent venous obstruction may lead to
chronic venous insufficiency and post –
thrombotic syndrome with associated pain,
edema, and ulceration of the affected limb.
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DISEASES OF THE VEINS:
THROMBUS FORMATION IN VEINS
▪ Prevention of DVT in at – risk individuals is important
and includes early ambulation, pneumatic devices, and
prophylactic anticoagulation.
▪ If thrombosis does occur, diagnosis is confirmed by a
combination serum D – dimer measurement and
Doppler ultrasonography.
▪ Management consists of anticoagulation therapy with
heparin and warfarin.
▪ In selected individuals, thrombolytic therapy or
placement of an inferior vena cava filter may be
indicated.
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DISEASES OF THE VEINS:
SUPERIOR VENA CAVA SYNDROME
▪ A progressive occlusion of the superior vena cava (SVC)
that leads to venous distention in the upper extremities
and head.
▪ Causes:
▪ Bronchogenic cancer (75% of cases).
▪ Lymphomas.
▪ Metastasis of other cancers.
▪ Tuberculosis.
▪ Mediastinal fibrosis.
▪ Cystic fibrosis
▪ Invasive therapies (pacemaker wires, central venous
catheters, and pulmonary artery catheters).
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DISEASES OF THE VEINS:
SUPERIOR VENA CAVA SYNDROME
▪ The SVC is a low pressure vessel that lies in the thoracic
compartment of the mediastinum.
▪ The right main stem bronchus abuts the SVC so that
cancers occurring in this bronchus may exert pressure on
the SVC.
▪ The SVC is surrounded by lymph nodes and lymph chains
that frequently become involved in thoracic cancers and
compress the SVC during tumor growth.
▪ Onset of SVCS is slow, so collateral venous drainage to
the azygos vein usually has time to develop.
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DISEASES OF THE VEINS:
SUPERIOR VENA CAVA SYNDROME
▪ CLINICAL MANIFESTATIONS: are edema and venous
distention in the upper extremities and face.
▪ Patients complain of a feeling of fullness in the head or
tightness of shirt collars, necklaces, and rings.
▪ Cerebral edema can cause headache, visual
disturbance, and impaired consciousness.
▪ Skin of the face and arms may become cyanotic and
taut.
▪ Capillary refill time is prolonged.
▪ Respiratory distress may be present because of edema
of bronchial structures or compression of the bronchus
by a carcinoma.
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DISEASES OF THE VEINS:
SUPERIOR VENA CAVA SYNDROME
▪ DIAGNOSIS: made by CXR, Doppler studies,
CT, MRI, and ultrasound.
▪ Not a vascular emergency due to its slow
onset and development of collateral
venous drainage.
▪ Considered an oncologic emergency if the
cause is from a cancer.
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DISEASES OF THE VEINS:
SUPERIOR VENA CAVA SYNDROME
▪ TREATMENT: for malignant disorders can
include radiation therapy, surgery,
chemotherapy, and the administration of
diuretics, steroids, and anticoagulants.
▪ Treatment for nonmalignant causes may
include bypass surgery using various grafts,
thrombolysis (both locally and
systemically), balloon angioplasty, and
placement of intravascular stents.
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A and B show orthogonal venograms in a 36-year-old
woman with a history of acute promyelocytic
leukemia who had undergone treatment with
chemotherapy via an indwelling subclavian catheter.
Fifteen months previously, following courses of
chemotherapy, she had developed SVC syndrome
and had balloon dilatation alone of the caval-atrial
junction. At this study, she presented with recurrent
SVC syndrome and there is restenosis at the site of
the prior venoplasty (arrows).
EUGENE PARDI, DO
The lesion in Figure 1 has been
crossed with a guidewire and
initial dilatation performed (A)
with a 12 mm × 40 mm XXL
balloon (Meditech-Boston
Scientific). Following balloon
dilatation, there was evidence of
elastic recoil and a Palmaz 308
stent was positioned across the
residual lesion (B). The small
arrows indicate the proximal and
distal ends of the stent. Stent
deployment was performed (C),
covering the lesion (arrow).
After postdilatation, the
expanded stent can be seen
in place and a pressure
gradient was measured (A).
Wide patency is
documented with
venography
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ HYPERTENSION (HTN) is consistent elevation of systemic
arterial blood pressure.
▪ The most common primary diagnosis in the United
States.
▪ One in three Americans has hypertension.
▪ > 2/3 of those older than 60 are affected.
▪ The chance of developing primary HTN increases with
age.
▪ HTN does occur in children & is being diagnosed with
increasing frequency.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ HTN is defined as a sustained systolic blood
pressure of 140 mm Hg or greater or a diastolic
pressure of 90 mm Hg or greater.
▪ All stages of HTN are associated with increased
risk for target organ disease events.
▪ MI, kidney disease, and stroke.
▪ Both stage I and stage II HTN need effective long
– term therapy.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ ISOLATED SYSTOLIC HYPERTENSION (ISH) defined as a
sustained systolic blood pressure (BP) that is ≥140 mm Hg
and a diastolic measurement that is < 90 mm Hg.
▪ ISH is strongly associated with cardiovascular and
cerebrovascular events.
▪ Most cases of HTN are diagnosed as PRIMARY
HYPERTENSION (also called ESSENTIAL or IDIOPATHIC
HYPERTENSION).
▪ 92% to 95% of hypertensive individuals have primary
disease.
▪ SECONDARY HYPERTENSION is caused by an underlying
disorder, such as renal disease.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HYPERTENSION: a combination of genetic and
environmental factors is responsible for its development.
▪ Genetic predisposition to HTN is believed to be
polygenic.
▪ Factors associated with primary HTN include:
▪ Family history of HTN.
▪ Advancing age.
▪ Gender (men younger than age 55; women after age
70).
▪ Black race.
▪ High dietary sodium intake.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ Factors associated with primary HTN (cont’d):
▪Glucose intolerance (insulin resistance and
diabetes mellitus).
▪Cigarette smoking.
▪Obesity.
▪Heavy alcohol consumption.
▪Low dietary intake of potassium, calcium, and
magnesium.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ Many of these factors are also risk factors
for other cardiovascular disorders.
▪Obesity, hypertension, dyslipidemia, and
glucose intolerance are found together in
a condition called the METABOLIC
SYNDROME.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪PRIMARY HTN (CONT’D):
▪PATHOPHYSIOLOGY:
▪Hypertension results from a sustained
increase in peripheral resistance
(arteriolar vasoconstriction), an
increase in circulating blood volume,
or both.
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DISEASES OF THE ARTERIES:
HYPERTENSION
•Primary HTN is the result of an interaction
of genetics and the environment.
•Multiple pathophysiologic mechanisms
mediate this interaction.
•The SNS, the renin – angiotensisn –
aldosterone system (RAAS), and the
natriuretic peptides.
PRIMARY HTN •Inflammation, endothelial dysfunction,
(CONT’D):
obesity – related hormones, and insulin
resistance contribute to both increased
peripheral resistance and increased
blood volume.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ Increased volume is related to a shift in the
PRESSURE – NATRIURESIS RELATIONSHIP.
▪For a given blood pressure, individuals with
HTN tend to secrete less salt in their urine.
▪ The SNS has been implicated in both the
development and the maintenance of elevated
blood pressure.
▪Also plays a role in hypertensive end organ
damage.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ Overactivity of the RAAS contributes to salt and water
retention and increased vascular resistance.
▪ High levels of angiotensin II contributes to endothelial
dysfunction, insulin resistance, and platelet aggregation.
▪ Angiotensin II mediates structural change in the vessel wall
resulting in permanent increases in peripheral resistance.
▪ Angiotensin II is associated with end – organ effects of HTN
▪ Atherosclerosis.
▪ Renal disease.
▪ Cardiac hypertrophy.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ Overactivity of the RAAS (CONT’D):
▪ Aldosterone contributes to sodium retention by the
kidney and has other deleterious effects on the
cardiovascular system.
▪ ANGIOTENSIN – CONVERTING ENZYME (ACE)
INHIBITORS and ANGIOTENSIN RECEPTOR
BLOCKERS (ARBs) oppose the activity of the RAAS
and are effective in reducing blood pressure and
protecting against target organ damage.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ The natriuretic hormones modulate renal
sodium (Na+) excretion and require
adequate K+, Ca++, and Mg++ to function
properly.
▪Atrial natriuretic peptide (ANP)
▪Brain natriuretic peptide (BNP)
▪C – type natriuretic peptide (CNP)
▪Urodilantin
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ In HTN, increased ANP and BNP levels are
linked to an increased risk for ventricular
hypertrophy, atherosclerosis, and heart
failure.
▪ Salt retention leads to water retention and
increased blood volume, which leads to an
increase in blood pressure.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ Inflammation plays a role in the pathogenesis
of HTN.
▪Chronic inflammation contributes to vascular
remodeling and smooth muscle contraction.
▪Endothelial injury and dysfunction leads to a
decreased production of vasodilators, NO2,
and an increased production of
vasoconstrictors, endothelin.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ Obesity is a risk factor for HTN in both adults
and children.
▪Causes changes in the ADIPOKINES (LEPTIN
and ADIPONECTIN) and is associated with
increased activity of the SNS and the RAAS.
▪Is linked to inflammation, endothelial
dysfunction, and insulin resistance and an
increased risk for cardiovascular
complications from HTN.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ PRIMARY HTN (CONT’D):
▪ Insulin resistance is common in HTN, even in individuals
without clinical diabetes.
▪ Associated with decreased endothelial release of NO2 and
other vasodilators.
▪ Insulin resistance also causes renal salt and water
retention.
▪ Is associated with Overactivity of the SNS and the RAAS.
▪ The interactions between obesity, HTN, insulin resistance,
and lipid disorders in the METABOLIC SYNDROME result in a
high risk of cardiovascular disease.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ SECONDARY HYPERTENSION: caused by an
underlying disease process or medication that
raises peripheral vascular resistance or cardiac
output.
▪ Renal vascular or parenchymal disease.
▪ Adrenocortical tumors.
▪ Adrenomedullary tumors (pheochromocytoma).
▪ Drugs (OCPs, corticosteroids, antihistamines).
▪ If the cause is removed or the drug discontinued
before permanent structural change occurs, BP
will return to normal.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ COMPLICATED HYPERTENSION: when the HTN
becomes more severe and chronic, tissue
damage can occur in the blood vessels and
tissues, leading to target organ damage in the
heart, kidney, brain, and eyes.
▪ CV complications include left ventricular
hypertrophy, angina pectoris, heart failure,
coronary artery disease, MI, and sudden death.
▪ Vascular complications include the formation,
dissection, and rupture of aneurysms and
atherosclerosis leading to vessel occlusion.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ COMPLICATED HYPERTENSION (CONT’D):
▪ Renal complications include parenchymal
damage, nephrosclerosis, renal
arteriosclerosis, and renal insufficiency or
failure.
▪MICROALBUMINURIA is an early sign of
impending renal dysfunction and
significantly increased risk for CV events,
especially in those who have DM.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪COMPLICATED HYPERTENSION
(CONT’D):
▪Complications specific to the retina
include retinal vascular sclerosis,
exudation, and hemorrhage.
▪Cerebrovascular complications include
TIA’s, stroke, cerebral thrombosis,
aneurysm, hemorrhage, and dementia.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ MALIGNANT HYPERTENSION: rapidly progressive
hypertension in which DIASTOLIC pressure is greater than
140 mm Hg (normal < 90 mm Hg).
▪ High arterial pressure renders the cerebral arterioles
incapable of regulating blood flow to the cerebral capillary
beds.
▪ Due to the high pressure, capillaries exude fluid into the
interstitial space.
▪ Cerebral edema and cerebral dysfunction
(ENCEPHALOPATHY) occurs and increases until death if the
HTN is not reduced.
▪ Organ damage from malignant HTN is life threatening.
▪ Malignant HTN can also cause papilledema, cardiac failure,
uremia, retinopathy, and CVA.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ CLINICAL MANIFESTATIONS: the early stages of
HTN have no clinical manifestations other than
elevated blood pressure.
▪ HTN is called a “silent disease”.
▪ If HTN is not detected or treated, it becomes
established and may begin to accelerate its
effects on tissues when the individual is 30 to
50 years of age.
▪ Complications of HTN begin to appear during the
fourth, fifth, and sixth decades of life
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ CLINICAL MANIFESTATIONS (CONT’D):
▪ Most clinical manifestations of hypertensive
disease are caused by complications that damage
organs and tissues outside the vascular system.
▪ Signs and symptoms are specific for the organs or
tissues affected.
▪ Heart disease, renal insufficiency, CNS
dysfunction, impaired vision, impair mobility,
vascular occlusion, or edema can all be caused by
sustained HTN.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ EVALUATION AND TREATMENT: diagnosis requires the
measurement of blood pressure on at least two separate
occasions, averaging two readings at least 2 minutes apart, with
the following conditions:
▪ The person is seated, the arm is supported at heart level, the
person must be at rest for at least 5 minutes, and the person
should not have smoked or ingested any caffeine in the previous
30 minutes.
▪ Diagnostic tests for a complete evaluation of HTN include:
▪ 24 – hour blood pressure monitoring in selected individuals.
▪ CBC, UA, biochemical blood profile (plasma glucose, sodium,
potassium, calcium, magnesium, creatinine, cholesterol with
fractions, and triglycerides).
▪ Electrocardiogram (ECG).
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ EVALUATION AND TREATMENT (CONT’D):
▪ If the initial diagnostic screening is negative for any
underlying disease, then the patient has essential
or primary HTN.
▪ Treatment of primary HTN depends on its severity.
▪ Life style modification is important for prevention of
HTN and as part of a treatment regimen.
▪ Modifications include an exercise program, dietary
modifications, stopping smoking, and losing
weight.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ EVALUATION AND TREATMENT (CONT’D):
▪ Pharmacologic treatment of HTN reduces the
risk of end – organ damage and prevents major
diseases (MI and CVA).
▪Diuretics have been effective in lowering BP
and preventing cardiovascular complications.
▪An ACE inhibitor, ARB, or aldosterone
antagonist might be effective in the patients in
heart failure, chronic kidney disease, or who
have a history of MI and stroke.
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DISEASES OF THE ARTERIES:
HYPERTENSION
▪ EVALUATION AND TREATMENT (CONT’D):
▪ Pharmacologic treatment (cont’d):
▪Some patients require two or more drugs
for BP control, including combinations of
diuretics and other antihypertensives,
such as beta blockers, calcium channel
blockers, and ACE inhibitors.
▪Careful follow – up to support continued
adherence, determine the response, and
monitor for side effects of these
medications is important.
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DISEASES OF THE ARTERIES:
HYPERTENSION
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DISEASES OF THE ARTERIES:
HYPERTENSION
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