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41 Cards in this Set

  • Front
  • Back
Complications of COPD
• Peptic Ulcers and Gastroesophageal Reflux
• Acute exacerbations
• Pneumonia
• Pneumothorax
• Acute respiratory failure
• Cor pulmonale
COPD cor pulmonale
Lung Volume Reduction Surgery
• What? – Removal of portions of lung
• Who? – People who can no longer be managed medically. No smoking >6 months
• Post op care similar to any chest surgery
– Emphasis on lung rehab and assessment
Pleural Space Disorders--• Pleural effusion
• Increased hydrostatic pressure (CHF)
• Reduced capillary oncotic pressure (liver or renal failure)
• Increased capillary permeability (infections)
• Impaired lymphatic function (lymph obstruction-tumor)
pleural effusion:manifestations
• Shortness of breath, chest pain
• Tachypnea, hypoxemia, pleural rub
• Pleural effusion
– Transudative vs. Exudative
– Treatment
• Primary
– Thoracentesis
• Recurrent
– Pleurodisis
• In COPD – rupture of an emphysematous bleb
• Spontaneous pneumothorax
• Air in pleural space
• Trauma
Pneumothorax: s/sx
• Sudden onset of pleuritic chest pain
– Dyspnea, shortness of breath, increased work of breathing
• Diagnostic test
Pneumothorax: tx
– Oxygen
– Possible placement of chest tube
Pleuritic Pain assessment:
• Assessment
– Location, quality, quantity, timing, Aggravating or relieving factors, associated manifestations
• Pulmonary embolism
Pulmonary embolism (PE) is an occlusion of a portion of the pulmonary blood vessels by an embolus. An embolus is a clot or other plug (thrombus) that is carried by the bloodstream from its point of origin to a smaller blood vessel, where it obstructs circulation. Depending on its size, an embolus can be lethal.
PE: manifestations
The clinical manifestations of PE are nonspecific and, in some clients, may not appear until late in the event. The most common manifestations of PE are tachypnea, dyspnea, anxiety or fretfulness, and chest pain. Hypoxemia may be present depending on the size of the embolism. Because these clinical manifestations are similar to those seen with myocardial infarction and other cardiovascular illnesses, overdiagnosis is as likely as underdiagnosis.
Pulmonary embolism: complications
Pulmonary embolism can lead to right-sided heart failure. Once the clot lodges, affected blood vessels in the lung collapse. This collapse increases the pressure in the pulmonary vasculature. The increased pressure increases the workload of the right side of the heart, leading to failure. Massive PE of the pulmonary artery can also result in cardiopulmonary collapse from lack of perfusion and resulting hypoxia and acidosis.
Pulmonary embolism:how the client is acting: s/sx
The client is usually dyspneic, especially if the embolus has occluded major arteries or major portions of lung tissue. Apprehension, cough, diaphoresis, syncope, and hemoptysis may occur. The presence of hemoptysis indicates that the infarction or areas of atelectasis have produced alveolar damage.

Respirations typically increase. Crackles, an accentuated second heart sound, tachycardia, and fever may also develop. Less common findings include heart gallops, edema, heart murmur, and cyanosis.
PE: dx tools
history and physical examination, supplemented by selective diagnostic tests. Pulse oximetry will be low and may be unresponsive to inhaled oxygen. ABG analysis indicates arterial hypoxemia (low PaO2) and hypocapnia (low PaCO2) in massive PE. Severe respiratory alkalosis may occur. Lactate dehydrogenase (LDH) isoenzymes show an increase in LDH3 if there is lung tissue injury. A chest radiograph may help to rule out other pulmonary diagnoses.
Definitive test for PE:
Pulmonary angiography remains the definitive means of diagnosis of PE (Figure 63-10). A radiopaque contrast agent is injected into the right atrium and pulmonary artery via a catheter threaded through a peripheral vein. Visualization of any filling defects of the heart and right pulmonary artery is achieved by taking sequential radiographs. Because of the invasive nature of the test, pulmonary angiography typically is reserved for cases in which the index of clinical suspicion is high despite nondiagnostic findings on other tests.
management of PE
dyspnea and anxiety in high-risk clients. Prompt recognition of the condition and immediate treatment are essential. Goals are to stabilize the cardiopulmonary system and reduce the threat of a further PE with anticoagulation therapy or trapping with an umbrella in the vena cava. For some clients, the clot can be lysed.
Sometimes hypoxemia can be reversed with lowflow oxygen by nasal cannula. Other clients may require endotracheal intubation to maintain PaO2 greater than 60 mm Hg. Hypotension is treated with fluids. If fluids do not raise the preload (right ventricular end-diastolic pressure) enough to raise blood pressure, inotropic agents may be required. Acidosis, which has a powerful vasoconstricting effect, is corrected with bicarbonate
Anticoagulant Therapy for PE
Typically, anticoagulation begins with IV standard (unfractionated) heparin sodium to reduce the risk of further clots and to prevent extension of existing clots.

In general, the initial target International Normalized Ratio should be 2.5 to 3.0. Administration of sodium warfarin is begun about 3 to 5 days before heparin is stopped to provide a transition to oral anticoagulation. Because the half-life of warfarin is long, about 2 to 3 days is required to achieve adequate anticoagulation. Clients are maintained on warfarin for 3 to 6 months.
Surgical Intervention for PE
Surgical interventions that may be used in treatment of PE include (1) vena cava interruption with the insertion of a filter (Figure 63-11) and (2) pulmonary embolectomy. The Greenfield filter, a basket-like cone of wires bent to look like an umbrella, is the most commonly used filter. The filter is inserted by threading it up the veins in the leg or neck until it reaches the vena cava at the level of the renal arteries. The filter allows blood flow while trapping emboli; however, vena cava filters are less effective than anticoagulation and may lead to deep vein thrombosis, and so these generally are used only when anticoagulants are contraindicated or ineffective.
Embolectomy is used in clients with significant hemodynamic instability caused by the embolus, especially those with unstable circulation and contraindications to thrombolytic therapy. An embolectomy involves surgical removal of emboli from the pulmonary arteries by either a thoracotomy or an embolectomy catheter.
Venous air embolism VAE
Venous air embolism (VAE) is the entry of air into the venous system. VAE may occur in any condition in which an open vein above the right atrium level is exposed to the atmosphere (e.g., trauma to a vein, insertion or removal of central venous catheters or pulmonary artery catheters, surgical procedures on the head and neck [e.g., craniotomy]), pelvic operations in Trendelenburg position, and during gas insufflation in laparoscopy.
VAE--venous air embolism can cause:
Entry of air into the venous system produces manifestations in the right ventricle, pulmonary circulation, or systemic circulation (if right-to-left shunts are present). Small amounts of air do not produce manifestations because air is removed from the circulation. Large boluses of air (3 to 8 ml/kg) can cause right ventricular outflow obstruction and result in cardiogenic shock and circulatory arrest.
manifestations of venous air embolism (similar to PE)
Manifestations develop immediately following embolization and are similar to pulmonary thromboembolism. The severity of manifestations is related to the degree of air entry. Manifestations include dyspnea, chest pain, mill wheel murmur upon auscultation of the heart, tachycardia, hypotension, decreased consciousness, circulatory shock, or sudden deat
If you suspect a VAE:
If VAE is suspected, any central line procedure in progress is immediately terminated and the line is clamped. Promptly place the client in Trendelenburg position and rotate toward the left lateral decubitus position. This maneuver helps trap air in the apex of the ventricle, prevents its ejection into the pulmonary arterial system, and maintains right ventricular output. The client is given 100% oxygen, and mechanical ventilation may be needed for significant respiratory distress or refractory hypoxemia.
Pulmonary hypertension definition:
Pulmonary hypertension is defined as a prolonged elevation of the mean pulmonary artery pressure (PAP) above 25 mm Hg at rest (normal, 10 to 20 mm Hg) or above 30 mm Hg during exercise (normal, 20 to 30 mm Hg).
Pulmonary hypertension classifications:
Severe forms of pulmonary hypertension are classified as either secondary or idiopathic (primary). Secondary pulmonary hypertension is usually associated with underlying heart or lung disease (e.g., PE, veno-occlusive disease, COPD). The cause of the idiopathic form is, by definition, unclear. It occurs most often in young adults between the ages of 30 and 40 years. Women are affected more often than men.1 The condition is progressive, leading to right-sided heart failure and severe dyspnea.
Pulmonary hypertension
Clinical Manifestations:
Clients with mild pulmonary hypertension may be relatively asymptomatic. In moderate to severe forms, the main (and occasionally only) manifestation is dyspnea. Fatigue, syncope, angina-like chest pain, palpitations, and muscular weakness also may occur.
Pulmonary hypertension drug tx
Vasodilator therapy is the cornerstone of pharmacologic management. First-line vasodilators used for treatment are the calcium channel antagonists nifedipine and diltiazem. For clients who do not respond to these drugs, prostacyclin (epoprostenol) therapy has been used and has been found to improve hemodynamic status and physical manifestations. Prostacyclin is a EB potent pulmonary vasodilator that also reduces right ventricular dilatation, prevents tricuspid regurgitation from worsening, and has antithrombotic properties related to its effects on platelets. Treatment with prostacyclin is expensive and difficult to manage because it requires long-term, continuous central infusion; however, an oral form of the drug, bosentan, has recently been introduced.
surgical tx of pulmonary htn
Some clients with severe pulmonary hypertension may undergo heart-lung, single, or bilateral-lung transplantation
prognosis of pulmonary htn:
The overall prognosis in severe pulmonary hypertension is poor, although treatment options are improving. This disorder has no known cure, but treatment of the underlying cause of secondary pulmonary hypertension may slow its progression. Supportive intervention with supplemental oxygen helps to reduce hypoxemia, whereas anticoagulants may be used to prevent thromboembolic events.
Cor Pulmonale
• Right ventricle enlarges with or without right-sided heart failure
• Caused by severe COPD, Pulmonary hypertension
• Improve ventilation with supplemental oxygen, chest physical therapy, and bronchial hygiene
Respiratory Failure
Failure of :
• Heart
• Pulmonary
• Vascular
Hypoxemic Respiratory Failure
Pulmonary Edema manifestations:
– ↑ RR, HR, & BP, dyspnea, frothy sputum
• Medical Management of hypoxemic resp failure:
– Correct Hypoxemia

– Reduce Preload

– Reduce Afterload

– Support Perfusion
nursing management of hypoxemic resp failure:
– Impaired Gas Exchange
• Assess vital signs and administer oxygen
• Upright position with legs dependent
• Medicate with morphine and nitroglycerin
– Fluid Volume Excess
• Medicate with diuretic- monitor K
• Monitor urine output, weight, vital signs
– Anxiety
Ventilatory Failure hallmark signs:
– ↑ CO2 → headache, dyspnea
– Resp ↑ (40-50) OR can fall
– Mental status changes
Ventilatory Failure management:
– Reverse Bronchospasm
– O2, NPPV (Non invasive positive pressure ventilation)
– Fix the problem
– Intubate and ventilate
Treatment of a PE
Movement prevents it, and treat with coumadin, after the heparin IV
Venous air embolism-- the cause is what??
3-8ml/kg of air in open vein above right atrium level. (quite a bit of air)
If you get a venous embolism, what do we do as nurses??
Terminate procedure, clamp central line, position in Trendelenberg and turn to left side. Give patient 100% oxygen. This will stop the air from going into the circulation of the heart and the lungs.
Vascular lung disease:
Cor Pulmonale-- right ventricle enlarges with or without right sided heart failure.
*Can by severe COPD, pulmonary hypertension
*Improve ventilation with supplemental oxygen, chest physical therapy, and bronchial hygeine.
Vascular lung disease:
Pulmonary hypertension--manifestations are SOB, fatique, chest pain, dizzy spells, and fainting.