Presentation on theme: "1. Interpret the pathophysiology of the topic into fundamental concepts. 2. Identify pertinent nursing assessments. 3. Discuss diagnostic testing associated."— Presentation transcript:
1. Interpret the pathophysiology of the topic into fundamental concepts. 2. Identify pertinent nursing assessments. 3. Discuss diagnostic testing associated with the case. 4. Illustrate case study topic with clinical examples. 5. Identify appropriate nursing diagnoses in priority order.
Sandra James is a 32 y. o. female with a history of varicose veins. She is a 5'2" and 150 lbs. Ms. James has two children ages 6 and 4. Her current method of birth control is oral contraceptives. She is currently hospitalized following excision of internal and external hemorrhoids. All other history is insignificant. Ms. James’post operative course is uneventful until the second day when she complains of pain in her left calf. On examination you find the calf swollen and warm to the touch L R. Homans sign is positive
You inform the primary physician and a doppler flow study is performed. The results reveal a left popliteal deep vein thrombosis. Ms. James is placed on bed rest and anticoagulation therapy via a continuous heparin infusion. She does well on heparin for 2 days after which she begins to c/o shortness of breath and left anteior chest pain that worsens with deep inspiration. She is restless and afraid and says, “Am I going to die?”
Physical assessment reveals the following: BP160/88 HR 120 Resp 34 and labored Temp 99EF
A stat chest x-ray showed left lower lobe atelectasis. Ms. James is started on O 2 via nasal cannula at 4 liters/min and an arterial blood gas is drawn. The following results are obtained: PH7.52 ↑ PaCO 2 28 ↑ PaO 2 131 SaO 2 99%
A ventilation perfusion scan performed that afternoon reveals perfusion defects of the anterior and posterior segments of the left upper lobe. Ventilation is normal, and a pulmonary embolus (PE) is suspected. Ms. James is scheduled for a pulmonary angiogram the next morning. On the morning of the scheduled angiogram, Ms. James PT and PTT are as follows: PT16.7 sec.PTT 46.9 sec. Control 1.7 sec. Control25.3 sec. INR
The angiogram is postponed pending reversal of the anticoagulation. Several hours later, Ms. James exhibits tachycardia, diaphoresis, and cyanosis. Her SaO 2, which is being monitored by pulse oximeter, drops to 81%. She is placed on a 100%nonrebreathing mask. An ABG is drawn after 30 min., and the results are as follows: pH7.48 PaCO 30 PaO 2 45 SaO 2 81%
Ms. James is intubated and placed on a volume ventilator. A moderate amount of blood-tinged secretions are suctioned from her endotracheal tube. A pulmonary angiogram done that day reveals emboli in the left upper lobe lingular and right main pulmonary arteries. Bilateral iliac vein Greenfield filters are placed under fluoroscopy and anticoagulation therapy is resumed. Once the prothrombin times are in the therapeutic range. Coumadin is started. Ms. James is extubated 24 hr after the filters are placed and the heparin is discontinued after 72 hr. She makes steady progress and is discharged on Coumadin therapy several days later.
Long term immobility Oral contraceptive use Estrogen therapy Smoking Hypercoagulability Obesity Surgery Heart failure Chronic Atrial fibrillation Autoimmune hemolytic anemia (sickle cell) Long bone fractures Advanced age
1. Fat Embolism: circulatory condition characterized by a plug of fat blocking an artery. The plug enters the circulatory system after the fracture of a long bone or traumatic injury to adipose tissue or to a fatty liver. Fat emboli are the result of the release of free fatty acids, causing a toxic vasculitis, followed by thrombosis, and obstruction of small pulmonary arteries by fat. Usually occurs within 12-36hrs after an injury. Risk Factors o multiple fractures o Males o Patients 10 – 39 years old o Trauma to adipose tissue or liver o Burns o Osteomyelitis o Sickle cell crisis
2. Air Embolism: the abnormal presence of air in the CV system resulting in obstruction of blood flow. May occur if large quantity of air is inadvertently introduced by injection (as during IV therapy or surgery) or by trauma (puncture wound) Risk Factors o Any surgical procedures that can lead to infusion of air o Creation of a pressure gradient of air entry (ex. Lumbar punctures, peripheral IVs, central venous catheter, etc.) o Positive pressure ventilation (during mechanical ventilation or scuba diving) o Blunt & penetrating trauma to the chest, abdomen, neck, or face can lead to entry of air Wittenberg, A.G. (2006). Venous air embolism. Retrieved February 6, 2008, from eMedicine WebMD on the World Wide Web: http://emedicine.medscape.com/article/761367- overview http://emedicine.medscape.com/article/761367- overview
3. Amniotic Fluid Emboli (AFE): occurs when amniotic fluid is drawn into the maternal circulation and carried to the woman’s lungs. Fetal particulate matter (skin cells, vernix, hair, and meconium) in the fluid obstructs pulmonary vessels. Failure of the right ventricle occurs early and can lead to hypoxemia. Left ventricle failure follows Risk Factors o medical induction of labor, o multiparity, o cesarean section or operative vaginal delivery, o abruption, o placenta previa, and o cervical laceration or uterine rupture
4. Thrombus: a condition in which a blood vessel is obstructed by a thrombus carried in the bloodstream from its site of formation. The area supplied by an obstructed artery may tingle & become cold, numb, and cyanotic. Thrombi can result from blood stasis, alterations in clotting factors, and injury to vessel walls. Risk Factors Immobility A-fib, heart failure/MI, rheumatic heart disease Prolonged surgery (longer than 30min) Pregnancy Postpartum period Trauma Mechanical ventilation Obesity Age > 55y/o
Wheezing Leg swelling Clammy or bluish-colored skin Excessive diaphoresis (sweating ) Anxiety, Feelings of dread Weak pulse Lightheadedness or fainting (syncope) Fever
The three classic signs of dyspnea, chest pain, and bloody cough (hemoptysis) only occur in 20% of patients The most common manifestations are anxiety and sudden onset of unexplained dyspnea, tachypnea, or tachycardia Another common finding is moderate hypoxemia with a low PaCO2 Crackles (Rales) and a sudden change in mental status as a result of hypoxemia are other manifestations
Massive emboli may result in sudden collapse of patient with shock, pallor, severe dyspnea, hypoxemia and crushing chest pain, although some with massive PE do not experience pain. The pulse is rapid and weak, low BP, and ECG shows right ventricular strain. When there is rapid obstruction of 50% or more of pulmonary vascular beds, corpulmonale may result since the right ventricle can't pump blood to the lungs. Medium sized emboli often cause pleuritic chest pain, dyspnea, slight fever, a productive cough with blood streaked sputum, and tachycardia and a pleural friction rub may be found upon examination. Small emboli usually go undetected or produce vague, transient symptoms. Repeated small emboli gradually cause a reduction in the capillary bed and eventually pulmonary hypertension.
History: 32 y.o. female with a history of varicose veins. 5’2 and 150 lbs (BMI: 27.4; Overweight is 25- 29.9) Patient is on oral contraceptives S.J. is being hospitalized following surgery for excision of internal and external hemorrhoids.
Left calf pain; swollen and warm to touch (L>R) Positive Homan’s Sign. Doppler Flow study a left popliteal DVT. Patient on Heparin.
Patient complains of shortness of breath and left anterior chest pain (worsens with deep inspiration) Patient is restless and afraid. Vital Signs: ◦ BP: 160/88 ◦ HR: 120 ◦ RR: 34 and labored ◦ Temp: 99° F
S.J. is intubated, moderate amount of blood tinged secretions are suctioned. Pulmonary angiogram reveals emboli in the left upper lobe lingular and right main pulmonary arteries.
Spiral CT scan Ventilation-Perfusion scan Pulmonary angiography Capnogram D-Dimer and Fibrin Degradation Cardiac Markers Venous Ultrasound Phosphorus Serum ABG Not diagnostic but help in diagnosing: Chest X-ray, history and physical examination, CBC count with WBC differential
Spiral CT is similar to the regular CT, but the spiral CT actually spirals around the body giving a 3D image. 1st line test for Pulmonary Embolism “The spiral CT scan is able to continuously rotate while obtaining slices and does not have to start and stop between each slice. This allows visualization of entire anatomic regions such as the lungs,”(Lewis et al.,599). Testing is quick and accurate, within 20 seconds. This type of visualization is helpful to identify if there is an emboli in either lung. Risks: exposure to radiation, allergic reaction to contrast medium
Most commonly used to test for PE Purpose: “test is used to identify areas of the lung not receiving ariflow or blood flow. Ventilation without perfusion suggests the probability of a pulmonary embolus,” (Lewis et al., p. 528) Two parts to the test: 1. Perfusion scan: Radioisotope IV injection. Scans to detect anything in the pulmonary circulation 2. Ventilation scan: Inhale radioactive gas (xenon). This displays how the gas within the lungs distributes. (Lewis et al., p. 599). “In the first part of the test, you inhale a small amount of radiopharmaceutical while a camera that’s able to detect radioactive substances takes pictures of the movement of air in your lungs. A small amount of a different radiopharmaceutical is then injected into a vein in your arm, and pictures are taken of blood flow in the blood vessels of your lungs,” (Mayoclinic.com, 2007) Testing: < 1hour
Type of test: Radiography Purpose : Used to confirm pulmonary embolism diagnosis. How it’s Done: Radio contrast is injected into the pulmonary artery or it ’ s branches. This is an invasive procedure. The patient is supine and a catheter is inserted via the antecubital or femoral vein to the left or the right of the pulmonary artery. Normal Findings: Pulmonary vessels fill symmetrically and quickly with no defects or obstruction. Risks: allergy to the contrast medium Dysrythmias Infection of the venous site
Type of test: Spectrometry Purpose: monitoring of exhaled CO2 levels. Decreased CO2 levels can be indicative of a pulmonary embolism. How it ’ s Done: The exhaled CO2 is measured with a gas analyzer. The analyzer is usually attached to the exhalation tube on a ventilator. Normal Findings: 35-45mm Hg Risks: none
Type of Test: Blood Purpose: D-dimer helps determine the presence of a clot when there is a diagnosis of deep vein thrombosis, DIC, or an acute M.I. How it ’ s Done: Venipuncture Normal Findings: D-dimers <0.5 mcg/mL Risks: none
Type of test: Serum Purpose: To determine if Creatine Kinase (CK) levels are elevated. Elevated CK can indicate a pulmonary embolism. How its Done: Blood is drawn by venipuncture at the bedside Normal findings: Adult male: 38-174 units Adult female: 26-140 units Risks: none
“A noninvasive “sonar” test known as a duplex venous ultrasonography, uses high- frequency sound waves to check for blood clots in your thigh veins,” (Mayoclinic.com, 2007). A transducer is used to transmit any sound waves found and provides an image on a computer screen. Test is fast and pain-free. (Mayoclinic.com, 2007)
Type of Test: Blood Purpose: Elevated levels of Serum phosphorus can indicate can indicate pulmonary embolism. How It ’ s Done: Venipuncture Normal Findings: Adult: 2.5-4.5mg/dL Risks: none
Type of Test: Arterial Blood Purpose: Shows whether a patient is experiencing Respiratory alkalosis, which can be indicative a pulmonary embolism. How it ’ s Done: Arterial blood sample is obtained via an arterial puncture or a arterial line. Normal Findings: pH: 7.35-7.45 pCO2: 35-45mm Hg HCO3: 21-28mEq pO2: 80-100mm Hg SaO2: adult >95% Base excess/deficit: +2 Risks: none
These tests are not considered diagnostic tests for a pulmonary embolism but help in the diagnostic process: ◦ Chest X-ray ◦ ECG monitoring ◦ CBC count with WBC differential ◦ History and Physical examination
Impaired gas exchange R/T altered oxygen supply S/T ventilation perfusion mismatch. Acute Pain R/T inflammatory process caused by thrombus formation. Risk for injury R/T hypercoagulable state. Ineffective protection R/T prolonged bleeding S/T anticoagulation therapy. Anxiety R/T pain and intrusive diagnostic and surgical tests and procedures.
Frequent ambulation Pneumatic Leg Compression Devices PT consult for immobile patients Pharmacologic interventions as per DOs Proper IV set up Patient education
Hypoxemia is a deficient oxygenation of the blood. A pulmonary embolism is a sudden blockage in a lung artery, most often caused by a traveling blood clot from a vein in the leg. These clots are formed via the condition of deep vein thrombosis.
A pulmonary embolism brings about lung tissue damage, hypoxia and other organ impairment as a result of your blood’s hypoxic state. Death can ensue. Other sources of embolism include Air embolism, Fat embolism, Amniotic fluid embolism, Septic embolism, Foreign body embolism and Tumor embolism.
Larger emboli can cause a reflex increase in ventilation (tachypnea), hypoxemia from ventilation/perfusion (V/Q) mismatch and shunting, atelectasis from alveolar hypocapnia and abnormalities in surfactant, and an increase in pulmonary vascular resistance caused by mechanical obstruction and vasoconstriction.
Sudden onset of dyspnea or tachypnea Tachycardia Sharp chest pain Restlessness and anxiety Nonproductive cough or hemoptysis Palpitations Nausea Syncope Mild to moderate hypoexmia with a low PaCO2
In most cases there are multiple emboli (Corrêa, i Cavalcanti, & Amaral Baruzzi, 2007).
The presentation of patients with PE can be categorized into 4 classes based on the acuity and severity of pulmonary arterial occlusion. (Sharma, 2006) ◦ Massive pulmonary embolism ◦ Acute pulmonary infarction ◦ Acute embolism without infarction: ◦ Multiple pulmonary emboli THE KEY POINT – THE BIGGER THE CLOT / OCCLUSION – THE WORSE THE SEVERITY
There is a predominant involvement of the lower lobes because they have a higher blood flow than the other lobes. (Lewis, SL., Heitkemper, MM., 2007)
(Lewis, Heitkemper, Dirksen, O’Brien, & Bucher, 599) 1. Prevent further growth or multiplication of thrombi in the lower extremities 2. Prevent embolization from the upper or lower extremities to the pulmonary vascular system 3. Provide cardiopulmonary support if indicated
Anticoagulant drugs are given to prevent existing blood clots from enlarging and additional clots from forming. Thrombolytic drugs break up and dissolve blood clots. Other Methods: ◦ Oxygen is given if blood oxygen levels are low. ◦ Analgesics are given to relieve pain. ◦ If blood pressure is low, intravenous fluids are given and sometimes drugs that increase blood pressure are given. ◦ Mechanical ventilation (a breathing tube) may be needed if respiratory failure develops.
Heparin is given intravenously to achieve a rapid effect, and doctors carefully regulate the dose. Doctors strive to achieve a full anticoagulant effect (targeted to an INR of 2.0 to 2.5 times normal) within the first 24 hours of treatment. Low-molecular-weight heparin is probably as effective as traditional heparin and does not require the blood test monitoring that is commonly recommended for conventional heparin. Warfarin, which also inhibits clotting but takes longer to start working, is given next. Because warfarin is taken by mouth, it can be used long-term. Heparin and warfarin are given together for 5 to 7 days, until blood tests show that the warfarin is effectively preventing clotting. Then, the heparin is discontinued.
Although both drugs decrease fibrin formation, they do so by different mechanisms: Heparin inactivates thrombin and factor Xa, whereas warfarin inhibits synthesis of clotting factors. Effects of heparin begin and fade rapidly, whereas effects of warfarin begin slowly but then persist for several days. Different tests are used to monitor therapy: PT is used to monitor warfarin: Normal range for the PT is between 10 and 13 sec. aPTT is used to monitor heparin: Normal range for aPTT is between 28 to 34 sec. Vitamin K is given to counteract warfarin whereas protamine is given to counteract heparin.
LMWHs are simply heparin preparations composed of molecules that are shorter than those found in unfractionated heparin. LMWHs are associated with a much lower incidence of heparin-induced thrombocytopenia than heparin and a lower incidence of osteoporosis. Administration of LMWHs is in a fixed dose by subcutaneous injection and don’t require aPTT monitoring, as opposed to heparin. As a result, LMW heparins can be used at home, an advance that would reduce cost and improve patient convenience.
How long anticoagulants are given depends on the person's situation. If pulmonary embolism is caused by a temporary risk factor, such as surgery, treatment is given for 2 to 3 months. If the cause is some longer-term problem, such as prolonged bed rest, treatment usually is given for 3 to 6 months, but sometimes it must continue indefinitely. For example, people who have recurrent pulmonary embolism, often because of a hereditary clotting disorder, usually take anticoagulants indefinitely. While taking warfarin, people periodically have to have a blood test to determine if the dose needs to be adjusted.
Changes in diet and use of other drugs may affect the degree of warfarin's anticoagulant effects. If excessive anticoagulation occurs, severe bleeding in a number of body organs can develop. Because many drugs can interact with warfarin, people who take anticoagulants should be sure to check with their doctor before taking any other drugs, including drugs that can be obtained without a prescription (over-the-counter drugs) ◦ Such as acetaminophen or aspirin, herbal preparations, and dietary supplements. Foods that are high in vitamin K (which affects blood clotting) ◦ Such as broccoli, spinach, kale, and other leafy green vegetables, liver, grapefruit and grapefruit juice, and green tea, may also need to be avoided.
Thrombolytic drugs such as streptokinase or tissue plasminogen activator (TPA) break up and dissolve blood clots. Thrombolysis is more expensive than anticoagulant therapy and is associated with a higher risk of bleeding, so its use should be restricted to patients who are likely to benefit from it. They can be used for people who appear to be in danger of dying of pulmonary embolism. However, except in the most dire situations, these drugs cannot be given to people who have had surgery in the preceding 2 weeks, are pregnant, have had a recent stroke, or tend to bleed excessively.
The fibrinolytic enzymes streptokinase, and Alteplase (tPA) accelerate the rate of dissolution of thrombi and emboli by converting plasminogen to plasmin, an enzyme that degrades the fibrin matrix of thrombi.
Depending on the severity of the pulmonary embolism and the patient’s ABG results, supplemental oxygen may be needed by mask or nasal cannula. In some cases, patients may even need endotracheal intubation and mechanical ventilation Perform nursing interventions to prevent or treat atelectasis and maintain perfusion
Inferior vena cava interruption Filters – most commonly used for procedure Ligation and external clips – rarely used Pulmonary embolectomy Surgery is performed to remove clot Another type of embolectomy involves an introduced catheter to remove the clot
Prior to the surgery, a pulmonary angiography should be performed to visualize or rule out an embolus A filter is placed into the inferior vena cava typically beneath the renal vein under fluoroscopic guidance The filter will prevent large clots from travelling to the lungs by mechanically blocking their migration There are several types of filters and they fall into two categories: Permanent or Retrievable
Indications - A patient that has a contraindication to anticoagulants, complications of anticoagulation therapy, or failure to anticoagulant therapy. Prophylactic measure for patients with complications where a small PE would have severe consequences Patient undergoing pulmonary embolectomy Contraindications – A thrombus in the inferior vena cava blocking possible placement Uncorrectable, severe coagulapathy Bacteremia - the presence of bacteria in the blood
Benefits – Short-term reduction of occurrence of PE in patients with DVT with a likely sequelae of PE High rate of long term patency Complications – (Retrieved from the British Journal of Haematology) Immediate - Misplacement (1-3%), Early - Insertion site thrombosis (8.5%), and Infection Late - Recurrent DVT (21%), IVC thrombosis (2- 10%), Post-thrombotic syndrome (15-40%), and IVC penetration (0.3%)
A rare procedure where a clot is surgically removed from the pulmonary system Preoperative angiography must be done to find and confirm the pulmonary embolism An emergent embolectomy may be indicated for a patient with a severe obstruction who did not respond to the usual therapy IVC filter is placed after embolectomy Lewis et al. mentions the mortality rate of the procedure is 50%.
Respiratory measures - 1. When atelectasis was found on the chest x-ray, she was placed on 4L/min of oxygen via nasal cannula 2. The next day, Ms. James has an oxygen saturation of 81%, her ABG results show that her PaO2 is 45, and she is showing sings of tachycardia, diaphoresis, and cyanosis. Because she has a suspected PE, she is intubated and placed on a volume ventilator. 3. Nursing actions are performed by suctioning the blood-tinged secretions from her endotracheal tube.
Surgical Intervention 1. Pulmonary angiogram is performed revealing an emboli in the left upper lobe lingular and right main pulmonary arteries 2. Bilateral iliac vein Greenfield filters are placed under fluoroscopy. o Bilateral – inserted on both left and right side o Fluoroscopy – use of x-rays to guide insertion o Greenfield filters – Permanent, stainless steel o Iliac vein:
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