Transcript Document

ACUTE
CIRCULATORY
DISORDERS
Ivano-Frankivsk Medical university
Department of anesthesiology and intensive
therapy
Theme urgency.
– Blood system connects together
functionally different bodies and systems
in interests of life-support of an organism
as single whole.
– The blood system carries out this function
co-ordinating concerning a homeostasis in
close unity with lymphatic system.
– Maintenance of an adequate blood-groove complex process which depends on
adequate functioning of heart, integrity of
a vascular network and exact balance
between curtailing and anticurtailing
systems of blood.
Infringement of blood
circulation
• The general frustration arise in all organism,
all system of blood circulation and are
connected with infringements of activity of
heart or changes of volume and physical and
chemical properties of blood.
• Local infringements are caused by structurally
functional damages of a vascular channel on
any of its(his) sites - in one body, a part of
body or a body part.
THE GENERAL INFRINGEMENTS
OF BLOOD CIRCULATION
• The general arterial full blood (hyperaemia
universalis arteriosa) ;
• The general venous full blood (hyperaemia
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universalis venosa) ;
The general anaemia - sharp and chronic;
Blood condensation;
Shock;
Dissemination intravascular curling of blood
(DVS-SYNDROME).
Sharp the general venous
hyperaemia Its reason can be:
• Myocardium heart attack;
• Sharp myocarditis;
• Sharp exudative pleurisy with superfluous
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accumulation pleural liquid, squeezing lungs;
High standing of a diaphragm (at a peritonitis),
limiting breath;
THE a pulmonary artery;
All kinds of asphyxia.
Left ventricle insufficiency - leads
to development of a cardiac
asthma and edema of lungs
• Attacks of an inspiratory dyspnea to which the
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physical or psychoemotional load precedes.
The beginning acute, at night or in the evening,
during a sleep.
The attack is preceded with palpitation
Shortage of fresh air
The patient to sit down
duration - from 0,5 o'clock till several o'clock.
After an attack sense of weakness.
Objectively:
• Cold sweat
• Acrocyanosis
• An inspiratory dyspnea
• Wet moished rhonchy and dry rhonchy
• A sputum mucous in a trace amount
• A cantering rhythm, accent of the second
tone on a pulmonary artery
• Arterial pressure in norm or is enlarged
• The attack is accompanied by a polyuria
Cardiac asthma is transformed to
an edema of lung:
• The dyspnea increases
• Respiration bubbling
• Tussis with excretion sputum with a blood
• Wet rhonchy large-caliber, sonorous,
propagate on center and top departments
of the lungs
• A cyanosis
• Veins of a neck are enlarged
• A cantering rhythm, tints deaf persons.
Acute management
• To the Patient attach sitting position with the
alighted legs, on top and bottom extremities
impose garrots. 10 - 15 minutes garrots take
out everyone and impose repeatedly after a
time-out.
• Introduce high-speed diuretic - Furosemidum
into 60 mg.
• Introduce Morphinum - 1,0 1 % or its
analogues: Fentanylum 2,0 ml., Droperidolum
2,0 ml
• These drugs cause decrease of a venous inflow
of a blood to heart, redistribution of a blood
from a small circle of a circulation in big.
Acute management
• Quickly reduce pressure: Pentaminum of 5 %
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1,0 ml. in 20 ml an isoosmotic solution.
Introduce before pressure decrease on 30 %,
but not below 100 - 95 mm. Hg.
The Oxygenotherapy, an aspiration through a
mask of pair alcohol of 20 %, through a nasal
catheter - 70 - 15 % of steams of alcohol, in the
form of a spray - 15 %. Sputum delete by
means of an aspirator.
In \v introduce high-speed cardiac glycosides: a
strophanthin of 0,05 % 0,3 ml. on 10 ml. an
isoosmotic solution.
Acute write ventricle insufficiency
It is developed by acute stagnation in the big circle
of a circulation:
• - A swelling of cervical veins;
• - Sharp and morbid augmentation of a liver;
• - Edemas on the inferior extremities;
• - Plus signs of disease which has led acute r\v
insufficiency: a pulmonary heart, a
thrombembolism of a pulmonary artery.
Acute vascular failure
• Syncope - an acute vascular failure with a
short-term loss of consciousness that is
caused by an acute anemia of a brain.
The basic signs:
• Unexpected or instant switching-off of consciousness for some
seconds till 1-2 minutes, is rare up to 5 minutes
• Before this it can be observed: delicacy, giddiness, a ear noise,
emptiness in a head, darkening in opinion of, paleness, a
sweating, nausea, a numbness of extremities.
• Objectively: paleness, a sweating, a cold snap of extremities,
small sphygmus speeded up, arterial pressure is depressed,
respiration infrequent, superficial, tendon jerks are conserved.
At a long syncope twitching of muscles of the face and
extremities can be observed convulsive, salivation strengthens.
• After a syncope state, during several hours’ delicacy, a
headache is observed.
Acute management at
syncope:
• Horizontal position with the raised inferior
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extremities;
To provide access of fresh air (to unbutton
clothes to air a room);
To impose with heaters to cover a blanket;
To moisten the face and a breast with cold
water;
To pound legs and arms cloth or a brush to yield
to smell cotton with spirit of ammonia;
Subcutaneously to introduce 1-2 ml.
Cordiaminum, 1мл. 10 % of solution of a
coffeine, 2 ml. Camphors;
After appearance of consciousness to give a
drink hot tea, coffee.
Collapse - more serious form of a vascular
failure which arises owing to disturbance of
a regulation of a vascular tonus.
Clinic of a collapse.
• The collapse arises as complication at pathological
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states and at serious diseases.
Falloff of arterial pressure (below 90 мм.рт.ст),
diastolic and pulse pressure;
Paleness of skin, a sweating, depression of
temperature;
Threadlike puls, falling off of veins, a mydriasis, its
flaccid reaction to light;
Retardation (but not loss) consciousnesses, a
desorientation;
The Oliguria or anuria;
Lungs: respiration vesicular with hard shade.
Acute management at a
collapse:
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Horizontal position of the patient with the alighted head;
To cover, put a heater to legs;
Massive inhalation of the wetted oxygen;
I\v slowly: - 0,3 - 0,5 ml. 1 % of solution of a phenylephine
hydrochloride in 10 ml 0,9 % from tonic solution, or i\v 1 ml.
0,1 % of solution of Noradrenalinum, or i\v 2 mg. Cordiaminum
in 20 ml. 40 % of a glucose, Atropinum i\v 0,1 % - 1 ml. (at a
collapse owing to conducting новокаинамида);
• At absence of effect i\v 200 ml. Polyglucinum with 1 ml 1 % of
solution of a phenylephine hydrochloride or 0,5 mg. 0,1 % of
Noradrenalinum;
• After normalization of arterial pressure, spend hospitalization to
chamber of an intensive care laying on a stretcher with drained
PULMONARY THROMBOEMBOLISM
• It is occlusion of PA by thrombi
which primary appear in veins of
great circulation or in right part
of the heart.
Clinical classification
• Lightning – development of symptoms
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throughout a minute
Sharp - development of symptoms
throughout several hours
Subsharp - development of symptoms
throughout several days
Relapsed - at repeatedly of main
symptoms
Erased
Clinical classification
Behind degree of defeat of a pulmonary
vessel:
• Deadly - occlusion of 75 % of a pulmonary
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vascular channel there are more
Massive - defeat is more than 50 % of a
pulmonary vascular channel
Sub massive - defeat is less than 50 % of
a pulmonary vascular channel
Small or small branches - defeat in суме is
less than 25 % of a pulmonary vascular
channel
PULMONARY THROMBOEMBOLISM
• Thrombi forming anywhere in the
venous circulation can embolize in the
lung.
• In practice more than 90% of clinically
significant emboli arise in the deep
veins of the legs and thighs and are
associated with venous stasis.
PULMONARY THROMBOEMBOLISM
• The clinical effects of
thromboembolism vary depending on the
volume of emboli and on the condition
of both the pulmonary and systemic
circulations.
PULMONARY THROMBOEMBOLISM
The effects of embolism on gas
exchange
1)increased dead space
ventilation,
2)pneumoconstriction,
3)impaired synthesis of
pulmonary surfactant
PULMONARY THROMBOEMBOLISM
• The ventilation of unprefused lung adds to
the work of breathing and produces
tachypnea and a sense of dyspnea.
• Some patients manifest asthma-like
wheezing.
• Impaired surfactant production is a
delayed effect that produces edema and
atelectasis.
PULMONARY THROMBOEMBOLISM
• Massive pulmonary embolism is a well-
recognized cause of sudden death, which
may be virtually instantaneous or extend
over a period of a few minutes.
• The major pulmonary arteries are distended
with clots that are often coiled or twisted
and bear the imprint of venous valves.
• The lung parenchyma shows little change
except congestion, which presumably
comes by way of the bronchial circulation.
Summary
• Occlusion of pulmonary arteries, are almost
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always embolic.
Thrombosis of pulmonary arteries, are rare and
occurs only in pulmonary hypertension and
pulmonary atherosclerosis.
More than 95 % of pulmonary emboli arise in
deep veins of legs.
Frequency of pulmonary embolism correlates
with a predisposition to thrombosis in the legs.
30% of the patients with severe burns, trauma
or fractures show pulmonary embolism at
autopsy.
Summary
• Large emboli impact in the major
pulmonary artery or astride the
bifurcation of the pulmonary artery
(saddle embolus).
• Emboli may cause instantaneous death.
• Emboli may cause cardiovascular collapse
Summary
• Hemodynamic compromise is secondary, not only
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to vascular obstruction, but also to reflex
vasoconstriction caused by such agents as
thromboxane A2+.
Small emboli may be clinically silent in patients
without cardiovascular failure.Emboli may cause
transient chest pain and sometimes haemoptysis
due to pulmonary hemorrhage.
Pulmonary hemorrhage is characterized by blood
in the alveoli, but there is no ischemic necrosis of
the pulmonary parenchyma .
Summary
• In patients with compromised pulmonary
circulation (Eg. cardiac failure), emboli
may give rise to infarction.
• Middle sized emboli occlude moderatesized peripheral pulmonary branches.
• In rare cases, multiple small emboli may
produce chronic cor-pulmonale and
eventually pulmonary hypertension and
vascular sclerosis.
Pulmonary Thromboembolism
• Fat embolism is the result of abrupt pressure changes
in the long bones, which rupture thin walled venous
sinuses and force marrow fat into them. It embolizes to
the lung. In addition, levels of plasma triglycerides, free
fatty acids, and lipase rise as part of the stress response.
Endothelial damage is caused by fatty acids released
from embolized fat and by mediators released during
associated blood coagulation. Fat emboli can be
recognized by ordinary histopathologic sections as
sharply delimited, empty-appearing capillary loops or
arterioles, but frozen sections stained for fat are required
for confirmation.
Pulmonary Thromboembolism
• Amniotic fluid emboli are a rare complication of
pregnancy. Infusion of amniotic fluid occurs during
tumultuous uterine contractions when the head is in the
birth canal. The amniotic fluid is forced through a
rupture in the chorion into the maternal veins,
precipitating severe dyspnea, tachypnea, and
hypotension. Disseminated intravascular coagulation is a
common consequence. At autopsy the lungs are
hemorrhagic. Squamous cells are lodged in the
arterioles. Amniotic debris also contains lipid and mucin,
which can be identified with appropriate stains.
Reportedly, the clinical diagnosis can be confirmed by
the demonstration of squamous cells in blood withdrawn
by pulmonary artery catheter.
Pulmonary Thromboembolism
• Air embolism can be produced during inspiration if negative
intrathoracic pressure draws air into an open vein, an event
most likely to happen during a neurosurgical or ear, nose, and
throat procedure in which the patient sits upright and the
operative wound is above the level of the heart. Air bubbles
become trapped in pulmonary arteries and right ventricle
where they mechanically impede blood flow. Reactions at the
gas-fluid interface trigger blood clotting and the accumulation
and activation of neutrophils. Small fibrin and platelet thrombi
are found in pulmonary arteries. The physiologic
consequences include transient airway constriction and
vasoconstriction with great increases in pulmonary vascular
resistance and pulmonary artery pressure. With large
emboli pulmonary edema, hypoxemia, systemic hypotension
and myocardial ischemia are seen. Fatalities have been
reported with embolism of 100 ml of air.
Pulmonary Thromboembolism
• Foreign-body embolism can result from introduction of foreign material
into the veins during medical procedures but is also common among
intravenous narcotic users. Particles of insoluble material added as “fillers”
to drugs intended for oral use embolizes to the lung and impact in
arterioles and small muscular arteries where they cause thrombosis and
proliferation of intimal cells. Often they migrate into the perivascular space
or interstitium where they give rise to foreign-body granulomas composed
of macrophages, multinucleated giant cells, and a few lymphocytes. The
process of migration appears to involve the production of granulomatous
response in the vascular wall with disintegration of muscle and elastic
tissue. In cases where lesions are not numerous, their detection is aided
by the use of polarizing filters, since cornstarch and talc, two of the
materials commonly used as fillers, are strongly birefringent. When the
vascular thrombosis is widespread, pulmonary hypertension results.
Lesions may resemble those of primary pulmonary hypertension,
particularly in view of the cellular proliferation induced by the foreign
material. Extensive interstitial granulomas can produce roentgenographic
nodularity and a restrictive ventilatory defect.
Circulatory Disorders
• Drugs used are to maintain, preserve or restore
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circulation
Anticoagulants & antiplatelets (antithrombotics),
thrombolytics, antilipemics, peripheral vasodilatiors
Anticoagulants - prevent formation of clots that inhibit
circulation
Antiplatelets - prevent platelet aggregation
Thrombolytics (clot busters) - attack/dissolve formed
clots
Antilipemics - decrease bld. lipid concentration
Peripheral vasodilators - promote dilation of vessels
narrowed by vasospasm
Circulatory Disorders Thrombus
Formation
• Clot is a Thrombus formed in an arterial
or venous vessel
• thrombophlebitis - Both inflammation and
clots are present
• Some thrombus can be superficial but it’s
the DVT that’s a concern  embolism to
lungs.
Circulatory Disorders Thrombus
Formation
• Arterial formation
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- begins w/ platelet
adhesion to arterial vessel wall  Adenosine
diphosphate (ADP) released from platelets 
more platelet aggregation  Bld. flow inhibited
 fibrin, platelets & RBC’s surround clot 
build up of size structure  occludes bld
vessels  tissue ischemia
The result of Arterial Thrombus is localized
tissue injury from lack of perfusion
Circulatory Disorders Thrombus
Formation
• Venous Formation - Usually from slow bld flow
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- Can occur rapidly Stagnation of the blood flow initiate
the coagulation cascade production of
fibrinenmeshes RBC’s & platelets to form the
thrombus. Venous thrombus has a long tail that can
break off to produce an embolus. These travel to
faraway sites then lodge  in lung (capillary level) 
inadequate O2 & CO2 exchange occur (ie. pulmonary
embolism & cerebral embolism)
Oral & parenteral anticoagulants (Heparin/Warfarin)
primarily act by preventing venous thrombosis
Antiplatelet drugs primarily act by preventing arterial
thrombosis
Circulatory Disorders Thrombus
Formation
• Hemostasis is the normal homeostatic process of blood
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clotting.
Clotting proteins normally circulate in an inactive state &
must be activated to form a fibrin clot. When there is a
trigger - inc. bld viscosity from bed rest & stasis - the
clotting cascade is activated.
Bld vessel injured  platelets adhering to site of injury
 release of ADP a platelet plug - is ex. of Intrinsic
clotting path.
Tissue injury (outside bld vessels) = extrinsic pathway
activated
Circulatory Disorders Thrombus
Formation
• Risk Factors for Deep Vein Thrombophlebitis and
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Thromboembolism
Three factors increasing risk
1) Stasis of venous flow,
2) damage of the endothelium(inner lining of vein), and
3) hypercoagulability of the blood.
Hx. of thrombophlebitis, abdominal & pelvic
surgery, Obesity, neoplasms (lung), CHF, Advanced
age, A-fib, vasospasm, Prolonged immobility (bedrest, long trip spinal cord injury, FX. hip), CVA MI
PG, post partum, Estrogen TX (oral contraceptives),
IV therapy, trauma, Sepsis, Venous cannulation,
Drug abuse, Cigarette smoking Excessive vit E
intake Hypercoagulable states (Polycythemia,
severe anemias, Dehydration or malnutrition),
Antithrombin III deficiency
Circulatory Disorders
Anticoagulants
• Inhibit clot formation - Do NOT dissolve clots
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already formed, but prophylactically prevent new
clots
Used in clients w/ venous/arterial disorders that
put them at inc. risk of clot formation
Venous = DVT & Pulmonary embolism
Arterial = Coronary thrombosis (MI), artificial
heart valves, CVA
Circulatory Disorders Heparin
• A natural substance in the liver that prevents clot
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formation.
Primary use is to prevent venous thrombosis that can
lead to pulmonary embolism (PE) or stroke
Combines w/ antithrombin III  inactivates thrombin
and other clotting factors then the conversion of
fibrinogen to fibrin doesn’t occur so the clot is
prevented
Poorly absorbed through GI mucosa - given SQ & IV
Prolongs clotting time - partial thromboplastin time
(PTT) & activated partial thromboplastin time (aPTT) both bld tests are monitored during therapy
Circulatory Disorders Heparin
• Use - DVT, PE, & CVA, Rx of clients w/ heart valve
prosthesis, during CV surgery, post op, during
hemodialysis
* Low doses = prophylactically to prevent DVT
* Full doses = treats a thromboembolism & promotes
neutralization of activated clotting factors = prevents
extension of thrombi & formation of emboli
* If started shortly after formation of a thrombus heparin will also prevent it from developing into an
insoluble stable thrombus = reduced tissue damage
Circulatory Disorders Heparin
• SE - Decreased platelet count =
thrombocytopenia
Hemorrhage - give protamine sulfate IV
(an
anticoagulant antagonist)
• DI - Inc. effects w/ ASA, NSAIDs,
thrombolytics
Dec. effect w/ NTG
Circulatory - LMWH
• Low Molecular Weight Heparins (LMWHs) -
recently introduced to prevent venous
thromboembolism
• Binds to Antithrombin III which inhibits the
synthesis of factor Xa & formation of thrombin
• - enoxaparin (Lovenox) & dalteparin
sodium (Fragmin)
• - more stable dose, lower risk of bleeding,
freq. lab monitoring not required
Circulatory Disorders
LMWHs
• Use - Prevention of DVT after hip & knee
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replacement surgery & abd. surgery
Can be administered at home
Administered SQ BID
Available in prefilled syringes w/ attached needles
Usually given in the abdomen
Average Rx is 7 to 14 days
Bleeding less likely to occur
DI - caution client not to take antiplatelet drugs
(ASA) during therapy
Circulatory Disorders
Warfarin (Coumadin)
• Action - Inhibits activity of vit. K required for the
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activation of clotting factors II, VII, IX, & X. Blocking
these factors prevents clot formation
Use - prophylactically to prevent venous thrombosis,
A. fib., PE, coronary occlusion, thrombophlebitis
Prolongs clotting time & is monitored by the lab bld.
tests prothrombin time (PT) & International
normalized ratio (INR) - usually before administering
the next dose until therapeutic levels are reached.
INR is 1.3 - 2.0 therapeutic levels on coumadin = 2.0
- 3.0
CIRCULATORY DISORDERS
Warfarin (Coumadin)
• INR is replacing the PT  INR more accurate.
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Need higher
levels for prosthetic heart
valves, cardiac valvular disease and recurrent
emboli.
PT not consistent lab to lab or reagents used.
PT is 1.5 – 2 times the reference value to be
therapeutic
Regular monitoring is required for the duration of
drug therapy
Warfarin is well absorbed through the G.I. tract.
Food decreases.
Circulatory Disorders
Antiplatelet Drugs
Aspirin, Dipyridamole (Persantine), Ticlopidine
(Ticlid)
abciximab (ReoPro), tirofiban (Aggrastat)
• Action: To prevent thrombosis in the arteries by
suppressing platelet aggregation via diff. methods
• Use: Prevention of MI/stroke for clients w/ family hx
- prevention of a repeat MI, stroke in clients having
TIA’s
• Persantine & Ticlid = similar to ASA but more
expensive
• ReoPro & Aggrastat = mainly for acute coronary
syndromes. Route = IV
Circulatory Disorders
Thormbolytics
• Thromboembolism - Occlusion of an artery or vein
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caused by a thrombus or embolus - results in ischemia
that causes necrosis of the tissue distal to the
obstructed area.
- it takes about 1 to 2 weeks for the blood clot to
disintegrate by natural fibrinolytic mechanisms
- if new thrombus dissolved quicker damage
minimized & bld flow restored faster  purpose of
therapy
Thrombolytics promote fibrinolytic mechanism
(convert plasminogen to plasmin & destroys the fibrin
in the clot) - administering a thrombolytic drug = clot
disintegrates
Circulatory Disorders
Thrombolytics
• Use = Acute MI - w/ in 4 hrs to dissolve clot &
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unblock artery, so decrease necrosis to myocardium
& hospital stay is decreased.
Other uses: Pulmonary embolism, DVT,
Noncoronary arterial occlusion
Streptokinase, Urokinase, Tissue plasminogen
activator (t-PA), anisoylated plasminogen
streptokinase activator complex (APSAC)
Streptokinase & Urokinase are enzymes that act to
convert plasminogen to plasmin
t-PA and APSAC activate plasminogen by acting
specifically on clot.
Circulatory Disorders
Antilipemics
• Used to Lower bld. lipid levels
• Cholesterol, triglycerides & phospholipids
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transported in the body bound to protein in
various amounts - chylomicrons, very lowdensity lipoproteins (VLDL), low-density
lipoproteins (LDL), high-density lipoproteins
(HDL) - more protein & less lipid (removes chol.
from bld. stream & deliver it to the liver)
VLDL & LDL contribute to atheroslerotic plaque
in bld vessels - composed of mainly cholesterol
& triglycerides
Circulatory Disorders
Antilipemics
• Nonpharmacologic = before drugs to dec. BP
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- Reduce saturated fats & chol intake in the diet
- Exercise
- Body wt. reduction
- Eliminate smoking
If drug therapy needs to be initiated, clients still
need to make lifestyle changes
Compliance an issue
Circulatory Disorders
Antilipemics
• Cholestyramine (Questran) - Powder form,
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Colestipol (Colestid) - a newer resin - both lower
chol.
Clofibrate (Atromid-S), gemfibrozil (Lopid) - fibric
acid derivatives effective in reducing triglyceride & VLDL
levels.
- Highly protein bound. do not take w/ anticoagulants compete
- Clofibrate - many side effects - dysrhythmias, angina
Nicotinic acid or niacin (vit B2) - reduces VLDL &
LDL - effective in dec. chol levels, Many SE’s
Circulatory Disorders
Antilipemics
• Statin drugs inhibit enzyme HMG CoA reductase in
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chol biosynthesis ( HMG CoA reductase inhibitors)
= Dec. the concentration of chol & dec. LDL & sl.
inc. in HDL
atorvastatin calcium (Lipitor), cerivastatin
(Baycol), fluvastatin (Lescol), lovastatin
(Mevacor) - SE = GI disturbances, headaches, muscle cramps
& tiredness (all complaints early in tx.)
- monitor serum liver enzymes
- Annual Eye exams d/t poss cataract formation
- Useful in
coronary artery disease (CAD) &
mortality rate
Circulatory Disorders
Antilipemics
• If therapy withdrawn, cholesterol levels return to
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pretreatment levels  lifetime commitment
Lovastatin is absorbed with food. High 1st hepatic
pass -50%
Onset and peak occurs in hours , but takes several
days to have a therapeutic effect. Duration is up
to 3 weeks.
NI Monitor blood lipid levels, liver functions, if GI
upset occurs have client take with sufficient water
or with meals.
Desired Lab Values = CHOL <200; triglyceride
<150; LDL < 130; HDL > 60
Circulatory Disorders
Peripheral Vasodilators
• Peripheral Vasodilators - Increase bld flow to
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extremities
Peripheral vascular disease is a problem in the
elderly
- Numbness & coolness of extremities,
intermittent claudication (pain/weakness of limb
when walking - symptoms absent at rest), poss.
leg ulcers
- Primary cause is hyperlipemia from
atherosclerosis & arteriosclerosis - arteries
become occluded
Circulatory Disorders
Peripheral Vasodilators
• Peripheral vasodilators more effective for disorders
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resulting from vasospasm (Raynaud’s disease) than
from vessel occlusion or arteriosclerosis
Vasodilators have diff. actions but all promote
vasodilation
Isoxsuprine (Vasodilan) - Beta-2 adrenergic
agonist - causes vasodilation on arteries w/in
skeletal muscles, bronchodilation may also occur
- SE = lightheadedness, dizziness, orthostatic
hypotension, tachycardia, GI distress
Circulatory Disorders
Peripheral Vasodilators
• Pentoxifylline (Trental) - an antihemorrheologic
agent - improves microcirculation & tissue perfusion
inc. in tissue O2. Not a vasodilator, but dilates rigid
arteriosclerotic bld vessels - arterioles, capillaries &
venules
- Use = clients w/ intermittent claudication
- Take w/ food
- Avoid smoking d/t nicotine increases
vasoconstriction