Pulmonary embolism

- Blockage of pulmonary arteries by:

o Thrombus
o Fat
o Air embolus
o Tumor tissue
- Mobile clots that do not stop moving until lodged at narrowed
part of the circulatory system
- The lower lobes of the lungs are more commonly affected, due
to higher blood flow
- Causes:
o Most PE’s arise from DVT
o Lethal PE most commonly originate in the femoral or
iliac veins
o Other sites of origin of PE include:
▪ Right side of heart (especially with a fib.)
▪ Upper extremities and the pelvic veins
o Right side clots will move to lungs (PE)
o Left side clots will move to brain (stroke)
- Risk factors:
o Immobility
o Surgery within past 3 months (especially pelvic and lower extremities)
o History of DVT
o Malignancy
o Obesity
o Oral contraceptives
o Hormone therapy
o Cigarette smoking
o Prolonged air travel
o Heart failure *
o Pregnancy
o Clotting disorders
- Signs and symptoms:
o Anxiety
o Sudden onset of unexplained dyspnea
o Tachypnea
o Tachycardia
o Sudden change in mental status as a result of hypoxemia (decreased oxygen to to
tissues)
o Other manifestations:
▪ Cough
▪ Pleuritic chest pain
▪ Hemoptysis (coughing blood)
▪ Crackles
▪ Fever
▪ Accentuation of the pulmonic heart sound
- Diagnostic studies:
o CT scan (with contrast) – most frequently used
o Chest x-ray (atelectasis, pleural effusion)
o Continuous ECG monitoring (ST-segment and T-wave changes) – not
diagnostic
o ABGs (arterial blood gases) – PAO2 is low, pH remains normal unless
hyperventilation – leads to respiratory alkalosis
o Venous ultrasound
o Ventilation-perfusion scan (ventilation refers to the flow of air into and out
of alveoli, perfusion refers to the flow of blood to alveolar capillaries)
- Complications:
o Pleural effusion
o Pulmonary hypertension
▪ From hypoxemia or involvement >50% of the area of the normal
pulmonary bed
▪ As a single event, an embolus does not cause pulmonary hypertension
unless it is massive. Recurrent emboli may result in chronic pulmonary
hypertension
- Pleural effusion:
o Fluid builds up in the layers of tissue that line the outside of your lungs and the
inside of your chest.
o Symptoms include chest pain, SOB, and dry cough.
- Pleural edema:
o Is excessive liquid accumulation in the tissue and air spaces (usually alveoli) of
the lungs.
o It leads to impaired gas exchange and may cause hypoxemia and respiratory
failure.
- Pulmonary hypertension:
o Type of high BP that affects the arteries in the
lungs and the right side of the heart.
o The damage slows blood flow through the lungs,
and BP in the lung arteries rises.
o The heart must work harder to pump blood
through the lungs. The extra effort eventually
causes the heart muscle to become weak and fail.
- Goals of care:
o Prevent further growth or multiplication of thrombi in the lower extremities.
o Prevent embolization from the upper or lower extremities to the pulmonary
vascular system.
o Provide cardiopulmonary support if indicated
▪ O2 by nasal prongs
▪ Turning, coughing, deep breathing, spirometry (prevent atelectasis)
▪ Intubation (severe cases)
▪ Is heart failure is present, diuretics are used
▪ Pain from pleural irritation or reduced coronary blood flow – opioids
(morphine)
- Prevention:
o Prevention of PE begins with prevention of VTE
o VTE prophylaxis includes:
▪ The use of sequential compression devices
▪ Early ambulation
▪ Prophylactic use of anticoagulant medications (heparin SC)
- Treatments:
o Heparin IV infusion
▪ High alert medication (risk of causing patient harm – 2 nurses verify)
▪ Therapeutic class: anticoagulants
▪ Pharm. Class: antithrombotic
▪ Heparin works to prevent future clots but does not dissolve existing clots
▪ Dosage of heparin is adjusted according to the activated partial
thromboplastin time (aPTT)
▪ aPTT, PT, INR, and CBC must be done before starting infusion and at
least once/day
▪ Reversal of heparin = protamine sulfate
▪ Complications: hemorrhaging, thrombocytopenia (low platelets), and
osteopenia (loss of bone density)
• Prevent bleeding, cuts, contact sports…

o Warfarin (coumadin)
▪ High alert medication
▪ Therapeutic class: anticoagulants
▪ Typically administered for 3-6 months
▪ Dosage of warfarin is determined by the INR
▪ For patients with PE, the dose of warfarin is titrated to a therapeutic
international normalized ratio (INR), usually a target range of 2.0-3.0
(normal range = 0.9-1.10)
- Treatment monitoring:
o Lab test – coagulation profile: PT, PTT, INR
o Prothrombin time (PT): normal range = 11.9-14.7 seconds
▪ Measures how quickly you blood clots
▪ Reference range is 10-13 seconds
o Partial thromboplastin time (PTT): normal range = 29.1-42.2 seconds
▪ Also measures the speed of clotting but is primarily used to determine if
heparin therapy is working
▪ Can also help detect bleeding disorders
▪ Several medications and medical conditions can affect PTT results
including INR
RESP 2

Pulmonary hypertension
- elevated pulmonary pressure resulting from an increase in
pulmonary vascular resistance to blood flow through small arteries
and arterioles
- Primary pulmonary hypertension (PPH):
o Rare, severe, and progressive disease
o Associated with a poor prognosis because there is no
definitive therapy
- Secondary pulmonary hypertension (SPH):
o Occurs when a primary disease causes a chronic increase in
pulmonary artery pressures
- It can develop due to:
o Parenchymal lung disease
o Left ventricular dysfunction
o Intracardiac shunts
o Chronic pulmonary thrombo-embolism
o Systemic connective tissue disease
- Different anatomical or vascular changes cause the
pulmonary hypertension
- Examples:
o COPD: loss of capillaries as a result of
alveolar wall damage
o Pulmonary fibrosis: stiffening of the
pulmonary vasculature (ex. connective
tissue disorders)
o Chronic emboli: obstruction of blood flow
- Clinical manifestations:
o Classic symptoms:
▪ Dyspnea on exertion and fatigue
▪ Exertional chest pain, dizziness, and
exertional syncope
o Symptoms related to the inability of cardiac output to increase in response to
increased O2 demand
o As the disease progresses – dyspnea at rest
o Pulmonary hypertension increases workload of right ventricle – results in right
ventricle hypertrophy (COR pulmonale) and eventually right heart failure
- Chest x-ray generally shows enlarged central pulmonary arteries and clear lung fields
- Echocardiogram usually reveals right ventricular hypertrophy
- Treatment:
o Treating underlying disorder
o Diuretic therapy: relieves dyspnea and peripheral edema (reduces right ventricular
volume overload)
o Anticoagulation therapy: recommended with severe pulmonary hypertension to
prevent thrombus formation and venous thrombosis
 o Vasodilator therapy: used to reduce right ventricular overload (dilating pulmonary
vessles)
o Calcium channel blockers: relax pulmonary arteries and decrease resistance and
pressure of these vessels
o Synthetic prostacyclin: promote pulmonary vasodilation and reduce pulmonary
vascular resistance and treatment of choice for select patients unresponsive to
calcium channel blockers

COR pulmonale
- Enlargement of the right ventricle secondary to disease of the lung,
thorax, or pulmonary circulation
o Most common cause is COPD
- Clinical manifestations:
o Dyspnea, chronic productive cough, wheezing, respirations,
retrosternal or substernal pain, fatigue
- Collaborative care
o Treatment of underlying conditions

Chest trauma and thoracic injuries

- Blunt trauma
o Body struck by blunt object
o External injury may appear minor can mask
life-threatening internal injuries
o Contrecoup trauma
- Penetrating trauma
o Foreign body impales or passes through the
body tissues (gunshot wound, stabbing)
- Emergency management:
o Pneumothorax (air in pleural space)
▪ Chest tube insertion with chest drainage system
o Hemothorax (blood in pleual space)
▪ Chest tube insertion with chest drainage system, autotransfusion of
collected blood, treatment of hypovolemia as necessary
o Tension pneumothorax (air in pleural space that does not escape)
▪ Medical emergency
▪ Needle decompression followed by chest tube insertion with chest
drainage system
o Flail chest (fracture of 2 or more adjacent ribs in 2 or more places with loss of
chest-wall stability)
▪ Stabilization of flail segment with intubation in some patients and taping
in others
▪ Oxygen therapy, treatment of associated injuries
o Cardiac tamponade (blood rapidly collects in pericardial sac, compresses
myocardium, prevents heart from pumping effectively)
▪ Medical emergency
▪ Pericardiocentesis with surgical repair as appropriate
Pneumothorax
- Presence of air in pleural space
- Types:
o Closed pneumothorax:
▪ Has no associated external wound. Most common form
is a spontaneous pneumothorax, no apparent
precipitating event.
▪ It is caused by the rupture of small blebs (air-filled
alveolar dilations <1cm in diameter on the edge of the
lung at the apex of the upper lobe or superior of the
lower lobe) on the visceral pleural space. The cause of the blebs is
unknown.
▪ Occurs most commonly in underweight male cigarette smokers between
20 and 40 years old. There is a tendency for this condition to recur.
o Open pneumothorax:
▪ Occurs when air enters the pleural space through an opening in the chest
wall
▪ Examples include stab or gunshot wounds and surgical thoracotomies
▪ Should be covered with a vented dressing, taped on 3 sides
o Tension pneumothorax:
▪ Pneumothorax with rapid accumulation of air in the pleural space, causing
severely high intrapleural pressures with resultant tension on the heart and
great vessels
▪ May result from either an open or closed pneumothorax
o Hemothorax:
▪ Accumulation of blood in intrapleural space
▪ Frequently found with open pneumothorax
▪ Causes: chest trauma, lung malignancy, complications of
anticoagulant therapy, pulmonary embolus, and tearing
of pleural adhesions
o Chylothorax
▪ Presence of lymphatic fluid in the pleural space because
of a leak in the thoracic duct
▪ Causes include trauma, surgical procedures, and
malignancy
▪ Function of the thoracic duct is to transport lymph back
into the circulatory system
▪ Thoracic duct is disrupted, and the chylous fluid, milky
white with high lipid content, fills the pleural space
▪ Total lymphatic flow through the thoracic duct is 1500-2400mL/day
▪ 50% will heal with conservative treatment (chest drainage, bowel rest, and
TPN)
▪ Surgery may be required (pleurodesis)
 - Clinical manifestations
o Small: mild tachycardia and dyspnea
o Large: respiratory distress, including shallow, rapid respirations, dyspnea, air
hunger, decreased oxygen saturation
- Collaborative care
o May resolve spontaneously
o Aspiration of pleural space
o Insertion of chest tube (water-seal drainage)

Fractured ribs
- Most common type of chest injury resulting from trauma
o Ribs 5-10 are most commonly fractured
- Clinical manifestations
o Pain (especially on inspiration) at the site of injury
- An important goal in treatment is to decrease pain so that the patient can breathe
adequately to promote good chest expansion

Frail chest
- Results from multiple rib fractures, causing instability of the chest wall
o The affected (frail) area will move paradoxically to the intact portion
of the chest during respiration
o During inspiration, the affected portion is sucked in, and during
expiration, it bulges out
o Prevents adequate ventilation of the lung in the injured area
- Initial therapy consists of adequate ventilation, administration of humidified
O2 administration of crystalloid IV solutions, and pain control
- Definitive therapy is to re-expand the lung and ensure adequate oxygenation

Chest tubes and pleural drainage

- Nursing management
o Routine milking or stripping of chest tubes to maintain patency is no longer
recommended because it can cause dangerously high intrapleural pressure and
damage to pleural tissue
o Clamping of chest tubes during transport or when the tube is accidentally
disconnected is no longer advocated, there is a danger of rapid accumulation of air
in the pleural space, causing tension pneumothorax
 - Complications
o Chest tube malposition
o Re-expansion pulmonary edema
o Vasovagal response with symptomatic hypotension
o Infection at the skin site
o Pneumonia
o Shoulder disuse
- Chest tube removal
o Removed when the lungs are re-expanded, and fluid drainage has ceased
▪ Suction is discontinued
▪ Gravity drainage

Thoracentesis
- Types
o Diagnostic
o Therapeutic
- Patient sits on the edge of a bed and leans forward over a bedside table
- 1000-1200mL of pleural fluid is removed at one time
- Rapid removal can result in hypotension, hypoxemia, or pulmonary edema
- Must monitor for pneumothorax post procedure

Heimlich valves
- Device that may be used to evacuate air from the pleural space
- Consists of a rubber flutter one-way valve within a rigid plastic tube
- Attached to the external end of chest tube
- Valve opens when:
o Pressure > atmospheric pressure
- Valve closes when:
o Pressure <= atmospheric pressure
- Usually used for emergency transport or in special home care situations

Small chest tubes: pigtails

- Used in selected patients because they are less traumatic
- The drains may be straight catheters or “pigtail” catheters
- If occluded, can be irrigated by the MD using sterile water
- This catheter can also be used for chemical pleurodesis
- System is not suitable for trauma or draining blood
- Smaller tube can become kinked, occluded, or dislodged more easily
- Small-bore chest tubes and Heimlich valves should be used with caution in
patients on mechanical ventilators – potential for rapid accumulation of air and a
tension pneumothorax
Arterial and venous blood gas
- Values provide valuable
information about a patient’s
acid-base status, the origin of
the imbalance, an idea of the
body’s ability to regulate pH,
and a reflection of the patient’s
overall oxygen status
- Steps to interpret blood gas
- Acid-base disturbances are diagnosed, and compensatory processes identified in 6 steps
o 1: determining whether the pH is acidotic or alkalotic
▪ Value of 7.4 is the starting point
▪ Values <7.4 is acidotic
▪ Values >7.4 is alkalotic
▪ If the pH is between 7.35 and 7.45, and the CO2, HCO3-, and arterial
partial pressure of oxygen (PAO2) are within normal limits, the ABG
values are normal
o 2: analyzing the arterial partial pressure of carbon dioxide (PACO2)
▪ To determine whether the patient has respiratory acidosis or alkalosis
▪ Levels of CO2 are controlled by the lungs, and CO2 is this considered the
respiratory component of the ABG
▪ High CO2 levels indicate acidosis, and low CO2 levels indicate alkalosis
o 3: analyzing the HCO3-
▪ To determine whether the patient has metabolic acidosis or alkalosis
▪ Levels of HCO3-, the metabolic component of the ABG value, are
controlled primarily by the kidneys
▪ High levels of HCO3- result in alkalosis, and low levels result in acidosis
o 4: determining whether the CO2 or the HCO3- level matches the acid or base
alteration of the pH
▪ If the pH is acidotic and the CO2 level is high (respiratory acidosis) but
the HCO3- level is high (metabolic alkalosis), the CO2 is the parameter
that matches the pH derangement. The patient’s acid-base imbalance
would be diagnosed as respiratory acidosis
o 5: decide is body is attempting to compensate for the pH change
▪ Is the parameter that does not match the pH is moving in the opposite
direction
▪ The body is attempting to compensate
▪ The body will not overcompensate for pH changes
▪ If both parameters match the pH, it is possible that a combined respiratory
or metabolic acidosis or alkalosis is present, for example, if the pH is
acidotic, the CO2 level is high (respiratory acidosis), and the HCO3- level
is low (metabolic acidosis), the patient’s underlying acid-base imbalance
is combined respiratory-metabolic acidosis
o 6: assessing PAO2 and O2 sat, if these are abnormal, hypoxemia is present