Respiratory Emergencies: Pulmonary Embolism

• These study notes covers respiratory emergencies, acute coronary syndrome, dysrhythmias/EKG, and shock

Pulmonary Embolism (PE)

• A PE is particulate matter collection that enters venous circulation and lodges in pulmonary vessels
• Virchow's triad includes blood flow stasis, endothelial injury, and hypercoagulability
• Blood flow stasis may be caused by prolonged sitting, post-operative state, fall risk, or lower extremity fractures
• Endothelial injury examples include surgery, trauma directly injuring blood vessels
• Hypercoagulability may be due to cancer, pregnancy, sickle cell disease, or polycythemia

Causes of PE

• Thrombus: blood clot (most common)
• Fat: femur fracture
• Air: improper IV priming or air bubbles from IM injections
• Oil: used for diagnostic testing
• Tumor cells
• Amniotic fluid and fetal debris
• Foreign objects: broken IV catheters
• Injected particles: mannitol
• Infected clots: from dirty or infected IV needles

Risk Factors for PE

• Prolonged immobilization
• Surgery, hip or knee replacement, trauma
• Estrogen therapy (birth control and hormone replacement)
• General and genetic conditions that increase blood clotting
• CVC, HF, and stroke
• Pregnancy up to 3 months postpartum
• Obesity
• Advancing age
• COVID-19, infection, cancer
• Smoking
• History of thromboembolism
• Atrial fibrillation (A Fib) due to stagnant blood flow

Prevention of PE

• Lifestyle changes (modifiable risk factors) can help prevent PE
• Smoking cessation is recommended, especially when using hormone replacement therapy (HRT). Nicotine increases the risk of clot formation leading to vasoconstriction
• Weight reduction is advised
• Increased physical activity is encouraged
• Drink enough water when traveling
• Change positions often while traveling
• Avoid crossing legs
• Get up from sitting position 5 minutes per hour
• Retrievable IVC filters are used for surgical patients at high risk where it prevents DVT from becoming PE as it blocks clots from moving
• Filters areplaced before any surgery requiring decreased mobility for a few days, and retrieved once the patient can walk around
• Often done for patients who cannot take VTE prophylaxis due to a history of HIT
• Those taking OCP should not smoke; OCPs are not preferred
• Prevent infections such as COVID
• Anticoagulant use for VTE prophylaxis decreases VTE by 50-80%

Clinical Probability (Wells Criteria)

• ≤4 = PE is unlikely

• 4 = PE is likely

• Signs and symptoms of DVT, extremity swelling, pain, discoloration, extremity warmth are 3 points
• Strong suspicion of PE, other diagnoses ruled out or less likely is 3 points
• Heart rate >100 is 1.5 points
• Immobilization for 3+ days or recent surgery (within 4 weeks) is 1.5 points
• History of DVT or PE is 1.5 points
• Hemoptysis is 1 point
• Malignancy is 1 point
• A high score is >6. A moderate score is 2-6. A low score is <2
• For simplified Wells criteria PE likely is >4 and PE unlikely is <4

Patient Safety for VTE

• Start passive and active range-of-motion exercises for the extremities of immobilized and postoperative patients
• Ambulate patients as soon as possible after surgery
• Use pneumatic compression devices after surgery as ordered
• Evaluate patients for the need of anticoagulant therapy
• Administer ordered prophylactic low-dose anticoagulant or antiplatelet drugs after specific surgical procedures as soon as surgical bleeding risk has subsided
• Teach patients to avoid tight garters, girdles, and constricting clothing
• Prevent pressure under the popliteal space by not placing pillows under the knees and using alternating pressure mattress
• Perform a comprehensive assessment of peripheral circulation at least once a shift
• Elevate the affected limb 20 degrees or more above the level of the heart to improve venous return, as appropriate
• Reposition the patient every 2 hours, or ambulate as tolerated
• Refrain from massaging leg muscles
• Instruct patients not to cross their legs
• Encourage smoking cessation

Key Features for PE and Lab Results

• Sudden onset of dyspnea
• Sharp, stabbing chest pain
• Apprehension, restlessness
• Feeling of impending doom
• Light-headedness
• Cough
• Hemoptysis
• Diaphoresis
• Tachypnea
• Crackles
• Pleural friction rub
• Tachycardia
• S3 or S4 heart sounds
• Fever, low grade
• Petechiae over chest and axillae
• Hypoxemia
• Tachypnea and dyspnea are early symptoms. Hypoxemia and hypoxia are late symptoms and does not occur in all patients
• Cough is dry or productive
• Pleuritic friction rub involves sharp, stabbing pain on inspiration (chest pain)
• Hemoptysis is blood cough which does not occur in all patients
• Tachycardia and hypoTN are the result of reduced tissue perfusion from pulmonary HTN
• Extra breath sounds may include clear, crackles, wheeze, or plural friction rub
• History is important to determine the cause of PE
• ABGs will be consistent with respiratory alkalosis then other changes will occur and hyperoxygenating due to tachypnea, causing low CO2
• Metabolic panel to rule out other causes of those symptoms, kidney, liver, potassium
• Troponin is elevated in MI
• BNP elevated in HF (occurs with ventricular stretch)
• D-dimer is elevated in the presence of a clot and used to rule out PE
• aPTT indicates Heparin
• Computed Tomography pulmonary angiography (CTPA) for diagnosis: can actually look at vessels and visualize clots and can rule out other mimicking conditions

Nursing Interventions for PE

• Call rapid response (RRT) for any sudden onset dyspnea and chest pain
• Apply O2 by nasal cannula or face mask if SpO2 <90%
• Raise HOB to promote lung expansion
• Reassure patient and communicate plan of action
• Apply tele monitoring and continuous pulse ox, obtain venous access
• Prepare for ABG measurement and other diagnostic testing
• Check VS q30min-2hr depending on pt, cardiac & resp assessment
• Assess chest for petechiae
• Administer anticoagulants of fibrinolytic therapy to prevent further clot formation
• Start Heparin right away because it acts quickly. This is used for 5-10 days
• Initiate Warfarin on day 1-2 of heparin & will be used concurrently. Takes several days to reach therapeutic levels
• Continue on oral anticoagulants following discharge for at least 3-6 wks or indefinitely depending on ongoing risk
• Institute bleeding precautions

PE Severity and Treatment Options

• Massive PE (high risk):
  • Less than 5% of cases
  • Mortality may be as high as 65%; most deaths occur due to shock within the first hour
  • In severe instances: severe hypotension (SBP <90 mm Hg for at least 15 minutes), cardiac arrest, severe bradycardia, shock, RV dysfunction, distress
  • CPR; inotropic or vasopressor support, intravenous fluids, systemic thrombolysis, catheter-directed treatment, surgical embolectomy, and a Vena cava filter may be used
• Submassive PE (intermediate risk):
  • Mortality is 5%-15%
  • Normotension, RV dysfunction, R bundle branch block, ST elevation or depression, T-wave inversion, elevated BNP or troponin
  • Treatment is controversial however thrombolytic therapy surgical reperfusion strategy is an option
  • Anticoagulation is optimal
  • A Vena cava filter may be used also
• Nonmassive PE (low risk):
  • Mortality <1%
  • Normotension and no RV dysfunction, and no elevation in BNP or troponin
  • Fibrinolytics not warranted
  • LMWH, DOAC, Warfarin and Vena cava filter may be used
  • Inpatient hospitalization not usually needed
• Age >80; HR > 110; Hx of cancer; systolic BP < 100; O2 < 90; Hx of CPD

PE Treatment

• Embolectomy: if fibrinolytic therapy cannot be used if the patient has a massive or multiple PE with shock or bleeding
• Percutaneous catheter directed therapy: used when there's contraindication to tPa to inject directly into blot
• IVC Filter: used over drugs in pts w bleeding on anticoags, have septic PE, and are ongoing surgical embolectomy
• Pharmacologic: anticoagulants (Heparin, Warfarin, DOACs) and thrombolytics
• Vasopressors (Epi/norepi/dopamine) for severe bradycardic/hypotensive patients. Positive inotropes (Dobutamine) to support cardiac function
• Non-pharmacologic: CPR if patient is in cardiac arrest; Oxygen therapy via nasal cannula or face mask; elevationg HOB
• Bleeding precaution; Home care management with lifestyle modifications (smoking cessation, weight management, activity)

Managing Complications from PE

• HypoTN occurs due to inadequate circulation in the left ventricle as results from pulmonary HTN which causes reduced forward blood flow -Increase CO and maintain BP. Administer fluids and medications -Vasopressors when hypoTN persists despite fluid resuscitation (Norepinephrine, epinephrine, dopamine) -Less vital organs suffer -Positive inotropes (dobutamine, milrinone) increase cardiac contractility with monitoring -Monitor for indicators of fluid adequacy – urine output, skin turgor, moisture of mucous membranes
• Bleeding: Ensure antidotes are always present with bleeding precautions -Ensuring correct dosage and timing of drug therapy and Assess CBC & coags -Monitor for signs of bruising/bleeding, occult blood, abdomen distention/firmness -Low platelets can suggest HIT due to the formation of anti-heparin antibodies which may cause a need for platelet transfusion
• Precaution for thrombocytopenia: Platelet <20,000 = spontaneous, uncontrolled bleeding & intracranial hemorrhage
• Avoid IM & venipunctures, and postpone procedures if PLT <50,000
• Don't forcefully blow nose, no enemas, soft bristle toothbrush and firm soles in shoes

Therapeutic Response to PE treatment

• Attains and maintains adequate gas exchange and oxygenation
• No hypovolemia and shock
• Remains free from bleeding episodes

Acute Respiratory Distress Syndrome (ARDS)

• ARDS causes ARF and refractory hypoxemia
• Hypoxemia persists with 100% O2 and the vent cannot force perfusion with PaO2 still low. Decreased pulmonary compliance and Dyspnea is a hallmark of resp failure
• Bilateral pulmonary compliance NOT related to HF where an echo will show if it's not related to HF
• Dense pulmonary infiltrates on X-rays
• Direct injury comes from direct injuries to the lung (pneumonia/COVID, aspiration, trauma, fat embolisms) and indirect injuries causes inflammation such as sepsis and shock along with burns, pancreatitis, and other injuries with release of inflammatory properties

ARDS patient at risk

• Patient with direct and indirect injury
• On tube feeding and have impaired swallowing causing aspiration
• Increased WOB
• Hyperpnea: deeper breaths than normal NOT related to rate
• Noisy respiration: cyanosis, pallor, retraction intercostally of substernally
• Lower partial pressure of aterial O2 even with Remain is low even on 100% oxygen or low PaO2/FiO2 ratio
• sputum and ground glass will show on chest X-rays

Pathophysiology of ARDS

• Triggered by systemic inflammatory response
• Alveolar capillary membrane leaks separating air in lungs from blood circulation
• End result is impaired gas exchange from thick exudate

Three phases of ARDS

• first week is exudative with dyspnea, fluid may build, surfactant is reduced, and refractory hypoxemia develops
• Next 2nd week is fibrosing alveolitis for the repair by lungs and systemic inflammation and hypertension can lead to MODS,
• The lung attempts to have Epithelia restoration can lead to poor pulmonary defects

Interventions for ARDS

• Intubation with mechanical ventilation PEEP or CPAP; monitor for tension pneumothorax
• Frequent Lung Sounds assesment
• Positioning: Prone and turn pt each 2 hrs
• Drug and Therapy is to give supportive care and Conservative FLuid care to prevent excess fluid in the lungs
• Provide nutrition to reduce respirator muscle function and tube feedings ASAP

Mechanical Ventilation in ARDS patients

• Maintains patent airway, removing secretions, ventilation
• High presure can force air in lungs; must establish airway
• used for patients that are Progressive alveolar with hyperventilation or after a Surgery
• Explain procedure and have equipment ready with positioning as golden Standards

Mechanical Ventilation Indications

• PTS need Intubation or tracheostomy
• hypoxemia Progressive alveolar with hyperventilation
• chest injury or head injury
• ards and temporary surgeries

Complication with ventilator

• hypotension , fluid retention, lung problems
• GI issue. Vent dependent and needs muscle deconditioning
• Nursing Care is ventilator bundle and patient education

Key medications for respiratory issues

• TNK and other fibrinolytic, with a monitor and ICU consideration
• Heparin: monitor and patient education

Acute Coronary Syndrome (ACS)

• CAD affects the coronary arteries becoming blocked and leading to ischemia or infarction
• Ischemia is insufficient O2 supply and leads to a NSTEMI while Infarction is cell death and can lead to a STEMI

Risk factors for CAD

• High LDL, Low HDL
• Obesity
• HTN, carbon minoxide
• Sedentary or genetics
• Exercise goals for prevention or 150 min and diets low in fats and sodium

Types of Agina

• Stable: short term chest pain with reduced symptoms and is treated with rest and nitroglycerin
• UNstable: exercise does not help and the EKG is present
• Myocardial INfarction is determined with an EKG where STEMI is 100% blockage

Signs and symptoms of Myocardial Infarction

• Angina is chest pain
• MI consist of pain in jaw and lasting more than 30 min

Diagnostic for MI and Angina

• History of pain and Physical such as EKG, VS and S3 heart assessment
• Troponin levels T and I
• Stress or echoes are needed to measure activity in the heart rate

How to diagnosis a MI

• CHEST xray and blood test
• Cardiac Cath removes clots

Key interventions for MI and Agina

• Managing angina
• Nitro 2 times and then morphine can help but watch out for lung changes
• Oxygenation is needed along with decreasing afterload

Drug therapy needed are all side effective

• APlattelets, aspirin and beta blockers should reduce Heart rate with daily administration

Additional Interventions After MI

• One is prescribed ACE w/in 20 hrs to reduce Vas constriction
• Check Potassium Levels
• Reduce blood thickerness with stats an fibrin

The THromb20

• THrombolytics, Heprin, RAAS
• oxygen, morphine
• beta blockers statins and salicylate

Use of Pci needs quick implementation

• 90 min standard to insert the stain and prevent closure with EKG assesment

After care includes assessing the MI with shock

• S and s are VS change and undiagonsed check is HIGH
• Non and vas is needed for a right or left heart failure and can use pulmonary intervention for the Swan catheter

Cardiac Care

• Prevent Hypo Tn With graft rewarming with infection control
• Asses pericar and watch for low BP

Cardiac issues

• alter and infect the heart
• Key signs are Chest pressure, Friction and wbc and EKH
• Monitor BP
• treat pain, and treat infection if precent

Shock

• The lack of flow to vitals
• Stages are hypovolemic with loss of blood and leads to fluid admn
• Next is cardiogenic where the pump fails and will need Vas support
• Obstructive is pressure on the heart/ vassel

Anphlatci Showl

• This leads to constrict and swelling so needs epi and can give cpr with intubabtion

Septic issue

• With infection the system is affected
• monitor VS AND Give meds and cool

Interventions with the different shock

• Check Blood
• support Vas pressors and air

Important meds to remember

• EPI is one need if anaphylactic like