Heart Failure
Heart Failure (HF): an abnormal clinical condition that describes impaired cardiac pumping resulting
in the characteristic pathophysiological changes of vasoconstriction and fluid retention.
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Associated with many cardiovascular conditions such as
o
Long standing HTN
o
CAD
o
AMI
HF is characterized by:
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Ventricular dysfunction
o
Reduced exercise tolerance
o
Diminished QOL
o
Shortened life expectancy
Etiology:
o
HTN
o
Diabetes
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Obesity
o
Smoking
o
Hyperlipidemia
HF can also be characterized by any interference with the normal mechanisms regulating CO
such as:
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Preload
o
Afterload
o
Myocardial contractility
o
Heart rate
o
Metabolic state
all lead to a decrease in ventricular functioning
Pathophysiology of Systolic Heart Failure
o
Most common type of HF
o
Results from the inability of the heart to pump blood
o
Caused by a defect in the ability of the ventricles to contract (systole) or by an increase
in afterload, or by a mechanical abnormality
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What happens:
o
The LV loses its ability to generate enough pressure to eject blood forward through the high
pressured aorta.
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The hallmark of systolic HF is a decrease in the LV ejection fraction (EF) (% of the total
amount of blood in the LV ejected during each ventricular contraction)
o
Normal EF is 55% of the total ventricular volume
o
What happens is that when the EF decreases there is left over blood volume sitting in the LV
which eventually fills up the left ventricle and continues to back up (remember the normal
circulation of the heart so you know where the blood will back up into).
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Systolic HF is caused then by:
o
Impaired contractility
o
Increase in afterload (increase resistance)
o
Cardiomyopathies
o
Mechanical abnormalities
Pathophysiology of Diastolic Failure (DF)
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Often referred to as HF with preserved systolic function
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It is an impaired ability of the ventricles to fill during diastole
o
Decreased filling of the ventricles will lead to a decrease SV
Diastolic Failure is characterized by
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High filling pressures which results in venous engorgement in both the pulmonary and
systemic vascular systems
o
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Is usually a result of left ventricular hypertrophy from chronic HTN or aortic stenosis.
Diagnosis of diastolic failure is made by
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Evidence of pulmonary congestion
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Pulmonary hypertension
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Ventricular hypertrophy
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Normal EF
Mixed Systolic & Diastolic Failure
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Have poor EF (<35)
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High pulmonary pressures
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Bi-ventricular failure
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The client will have
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Low BP
o
Decreased CO
o
Poor renal perfusion
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Poor exercise intolerance
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Compensatory Mechanisms
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HF can have an abrupt onset s with a AMI or can be an insidious onset
o
The overload of the heart resorts to certain compensatory mechanisms to try to
maintain effective CO
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The main compensatory mechanisms are:
1. Ventricular dilation
2. Ventricular hypertrophy
3. Increase in SNS stimulation
4. Neurohormonal responses (RAAS and endothelin & natriuretic peptides)
Ventricular Dilation
o
Enlargement of the chambers of the heart occurs when the pressures in the heart chambers
(usually LV) is increased overtime
↓
o
The muscle fibres of the heart stretch in response to the volume of blood in the heart at the end
of diastole
↓
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The degree of stretch is directly related to the force of the contraction (Starling’s Law)
↓
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In the beginning dilation is an adaptive mechanism to cope with the increased blood volume and
increase in contraction leads to an increase in CO & maintenance of the arterial BP and
perfusion by the heart
o
Overtime however the elastic elements of the muscle fibers are over stretched and can no
longer contract effectively or efficiently so the CO diminishes
Ventricular Hypertrophy
o
Is an increase in the muscle mass & cardiac wall thickness in response to the overworked &
strain of chronic HF
o
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This increase in muscle mass & cardiac wall thickening happens slowly because it takes time for
this muscle tissue to develop
o
Hypertrophy usually follows the compensatory mechanism of ventricle dilation which further
increases the contractile power of the muscle fibres
↓
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This will lead to an increase CO & maintenance of tissue perfusion
o
The hypertrophic heart muscle however has poor contractility, and requires more 02 to
perform; has poor coronary artery circulation & is prone to ventricular dysrhythmias
SNS Activation
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Often the first mechanism triggered in low CO, but it is the least effective compensatory
mechanism
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When there is a decrease in SV/CO……there is an increase in epinephrine & nor-epinephrine
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This increases HR, myocardial contractility & peripheral vascular resistance (constriction)
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In the beginning contractility & CO are improved with the increased HR but overtime
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These factors are counter-productive instead increasing the myocardium need for 02 and the
workload of an already failing heart
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Vasoconstriction causes an immediate increase in preload which may increase CO initially but an
increase in the venous return to the heart where there is already volume overload worsens
ventricular performance
Neurohormonal Response
A. As CO decreases--- decreased perfusion to the kidneys
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Juxtaglomerular apparatus in the kidney senses the low blood volume and stimulates the kidney
to release renin which converts AT 1 to AT 2 by ACE
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AT 2 does two things: (a) causes peripheral vasoconstriction in order to increase BP
(b) overtime causes aldosterone to be released from the adrenal cortex which will increase Na &
H2O retention
B. Endothelin produced by the vascular endothelial cells is stimulated by ADH, catecholamines &
AT2
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Endothelin resultsn further arterial vasoconstriction & increases cardiac contractility &
ventricular hypertrophy
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The body’s ability to try to maintain balance is demonstrated by counter-regulatory process such as
atrial natriuretic peptide & brain natriuretic peptide which are both hormones produced by the
heart muscle that promote venous and atrial vasodilation (which will decrease afterload & preload)
Types of Heart Failure
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Left Sided: trace the blood backward from the LV to find out where the blood volume will
accumulate…..this will then allow you to think of the manifestations the patient can experience
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Right Sided: continue to trace the blood backward from where left sided heart failure lead you as
most commonly the cause of RF is LF. Think of the manifestations that will result because of this.
Left Sided Failure from an Increase in SVR (Lewis, et.al., 2013. p. 932)
Clinical Manifestations of Acute Decompensated HF (ADHF)
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Regardless of cause ADHF typically manifests as pulmonary edema
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Lung alveoli fill with serous or serosanguinous fluid
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In most cases of ADHF there is an increase in pulmonary venous pressure caused by
decreased efficiency in the LV
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Results in engorgement of the pulmonary vascular system
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Lungs become less compliant
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Which increase resistance in small airways
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If pulmonary pressures continue to increase there will be an increase in intravascular
pressure which will cause the fluid to move into the interstitial space which will be to
much for the lymphatics can drain.
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This will cause interstitial edema which will increase RR &SOBOE & at rest
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If pulmonary venous pressures continue to increase the cells of the alveoli’s lining
become disrupted & fluid containing RBCs moves into the alveoli- which translates to
fluid with fluid (in the alveoli & airways) which will worsen breathing and gas exchange
Diagnostic Tests for HF
1. History & PE
2. ABG’S, electrolytes, LFTs, BNP, cardiac enzymes
3. CXR
4. ECG
5. Echo, stress test, cardiac catheterization
Collaborative Care
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When we look how to treat patients with chronic CHF we first have to have a plan:
1. Identify the type of CHF they have & the causes
2. Correct sodium & water retention
3. Reduce the amount of work by the heart
4. Improve myocardial contractility
5. Control for factors that could precipitate an acute episode & those that could complicate the
CHF
6. Improve symptoms, minimize side effects
7. Prevent morbidity & prolong life
Pharmacological Considerations:
1. ACE inhibitors (drugs ending in “pril”)
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Used to treat systolic & diastolic heart failure
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First line treatment for acute episodes of CHF
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The drug works by preventing angiotensin 1 from converting to angiotensin 2 (which is potent
vasoconstrictor & sets up the release of aldosterone from adrenal cortex) an ACE will block this
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ACE inhibitors also decrease:
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SVR allowing for greater CO
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Pulmonary artery pressures
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Right atrial pressures
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LV filling pressures
Beta Blockers
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Can be started on patients who cannot take ACE inhibitors or in combination with other
drugs such as digoxin, diuretics
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Only 3 beta blockers are considered for treating pt’s with CHF (carvedilol and long acting
metoprolol & bisoprolol)
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“They directly block the SNS’s negative effects on the failing heart such as increased heart
rate”
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B-blockers must be started gradually and dose increased slowly every 2 weeks & proceed
slowly (and tolerated by pt)
Diuretic Therapy
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Indicated for patients with fluid retention
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They interfere with heart failure-induced sodium retention; inhibiting sodium or chloride
reabsorption in the renal tubules & excrete water (↓ amount of blood returning to the heart)
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Loop diuretics (Lasix) affect the loop of Henle are the best diuretics for failure patients because
they excrete sodium by up to 25% and remain effective until renal function is severely impaired
(Chojnowski, 2006)
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Can produce rapid results, improving cardiac function, subsiding symptoms & improving the
patients ability to tolerate exercise
Inotropic Medications
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Digoxin or digitalis increases myocardial contractility and reduces sodium reabsorption by the
renal tubules
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Increasing myocardial contractility increases CO, decreases LV diastolic pressure & decreases
SVR
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They have a positive inotropic action (strengthens contractility of the myocardium) and a
negative chronotropic action (slow heart rate)
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This allows for more complete emptying of the ventricles during diastole
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CO improves because of increased SV secondary to improved contractility
Vasodilators
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Goals according to Lewis, 2013 are
1. Increase venous capacity
2. Improve ejection fraction by improving ventricular contraction
3. Slows ventricular dysfunction
4. Decreases heart size
5. Avoids stimulation of neurohormonal responses initiated by the compensatory mechanisms of
CHF
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Major hemodynamic effect of nitrates is to decrease the preload
Deep Vein Thrombosis (DVT)
Is a disorder involving a thrombus in a deep vein (often iliac or femoral)
Etiology
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Three important factors called (Virchow’s Triad) as part of the etiology of DVT
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Venous stasis
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Intima (Endothelial) damage (inner lining of the vein)
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Hypercoagulability of the blood
Venous Stasis
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Normal blood flow in the venous system depends on the action of muscles in the extremities & the
functional adequacy of venous valves, which allow for blood flow in occur in one direction
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Stasis occurs when valve are dysfunctional or the muscles of the extremities are inactive
Intimal (Endothelial) Damage
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Damage to the endothelial surface of the vein maybe caused by trauma or external pressure &
occurs anytime venipuncture is performed.
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Damaged endothelium has ↓ fibrinolytic properties which predisposes thrombus development by
releasing clotting factors and activating platelets
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Some factors that predispose a vein to endothelial damage is:
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IV in for more than 48 hours
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Irritating IV substances (some medications, electrolyte additives)
Hypercoagulability of the Blood
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Occurs in many hematological conditions where the blood becomes ‘thick’ which predisposes
the blood to clot and there is an increase in fibrin production
Pathophysiology of DVT
RBCs, WBCs, platelets & fibrin aggregate & adhere especially at the vein cusps to form a thrombus
Clotting factors stimulate the production of fibrin which then traps the RBCs/WBCs/platelets to adhere
to the vein wall
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Frequent sites for DVT is in the cusps of veins where venous stasis allows accumulation of blood
products
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A thrombus enlarges, increases the number of blood cells & fibrin collects behind it to form a clot with a
tail
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Eventually the thrombus occludes the vein lumen (if partially occludes the thrombus gets covered by
endothelial cells and the thrombolytic process stops.
If the thrombus does not detach it undergoes lysis or becomes firmly organized & adherent within 5-7
days.
Organized thrombi may detach & turn into an emboli (usually because of the turbulent blood flow
within the vein at the site of the thrombus)
Manifestations of DVT
Diagnostic Studies
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History & PE
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Venous Doppler
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Duplex scan (U/S & Doppler)
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Blood tests (d-diamer, INR, platelets)
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Venogram
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Spiral CT
Collaborative Care
Prevention & Prophylaxis
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Focus is on the risk factors
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i.e after surgery what should patients do?
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If patient is on bed rest what should happen?
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If patient at risk for having decreased venous return to the heart what can they wear?
Pharmacological Means
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Anticoagulants used to prevent propagation (the spreading) of a clot, development of any new
thrombi or emboli
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Does not dissolve a clot!
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What are some anticoagulants you know?
Complications
Pulmonary Embolism
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Is the blockage of the pulmonary artery by thombus, fat or air emboli or neoplastic tissue
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Most PE’s arise from thrombi in the deep veins of the legs
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Other areas that can result in a PE is from the right side of the heart secondary to atrial
fibrillation (during MI), pelvic veins especially after surgery or childbirth
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Emboli are mobile clots that usually do not stop moving until they are lodged at a narrowed part
of the circulatory system
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Lungs are an ideal location because of their intensive arterial and capillary network
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Lower lobes of the lung is most often affected because they have higher blood flow than other
lobes
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Thrombi in the deep veins of the dislodge spontaneously, however more commonly a thrombus
is dislodged by a sudden mechanical force such as standing and changes in the rate of blood
flow such as the Valsalva manoeuver
Clinical Manifestations
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The severity of the manifestations depends on the size of the emboli and the size and number of
blood vessels occluded
 Anxiety
 Sudden onset of unexplained dyspnea
 Tachypnea or tachycardia
Other manifestations may include:
 Cough
hemoptysis
 Pleuretic chest pain
chest pain
 Fever
hightened pulmonic heart sound
 Sudden change in LOC
Severe Manifestations
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Can cause sudden collapse of client with PE
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Shock
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Pallor
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Severe dyspnea
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Crushing chest pain (some don’t have)
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↑ HR but weak & thready
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↓ BP
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Cor pulmonale
Collaborative Care
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Oxygen by mask
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May require intubation
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Continuous heparin infusion
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Coumadin for long term therapy
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Bedrest
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Narcotics for pain relief
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Thrombolytics
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Intracaval filters
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Pulmonary embolectomy in life threatening situations