Respiratory Disorders

PE Diagnostics

- ECG - noninvasive scintigraphic lung scan (ventila-tion/perfusion scan) is done to calculate pulmonary air flow and blood flow. - Helical (spi-ral) computed tomography is highly accurate for direct visualization of large emboli in the main or lobar pulmonary arteries, but it requires a 20- to 30-secondbreath-hold,which may not be feasible inpatients who are in unstable condition.

Nursing Support for ARDS

- O2 support - Circulation support (fluids, vasos) - Trend labs (ABGs, CBC, Chem panel, Xrays)

Priorities Post MVA case: •72yo Asian male 1900 to ER, wearing seatbelt, 25mph, T-bone to driver side, in C-Spine precautions. •Initial assessment: AAOx3, MAE, no external bleeding/ extremity fractures •c/o inspiratory pain right chest upper abdominal pain 6/10 •Initial VS: 104,149/79,28,37.1, 91% 2LNC

- O2 therapy - WOB - Is chest moving symmetrically - Chest xray - CT - ABGs - Hgb/Hct - CBC - we will trend over time - Chem 7 at least - Creatinine/BUN - Coagulation Panel - PT, aPTT, INR, platelets and fibrinogen

Allergy Nursing Interventions

1. Stop exposure 2. Initiate frequent VS 3. Monitor airway/lung sounds 4. Assess for rash/hives/swelling 5. Administer O2 & meds (benadryl, epinephrine, solumedrol) 6. Establish IV access call RT (ask for albuterol) continuous pulse oximetry continuous BP EKG Priorities: Airway support establish IV access (NS) Anti-histamine (epi) Q5m checks

air leak indicator timeline

1. will start with bubbles due to leak in lungs 2. bubbles will subside over time 3. once subsided you know air leak in lungs has resolved 4. clamp chest tubes for ~3 hrs to see how pt tolerates it/chest xray to see if lungs are healed

O2 support for extreme respiratory distress

100% NRB Bipap - does not qualify due to facial trauma Intubation - she needs to be intubated

Duplex Ultrasonography

95% sensitivity and specificity for detecting deep venousthrombosis above knee

Pulmonary Embolism

A blood clot that breaks off from a large vein and travels to the blood vessels of the lung, causing obstruction of blood flow. leading cause of maternal death after a livebirth main symptom of pulmonaryembolism is often a vague complaintof dyspnea or chest pain, and deathcommonly occurs within 1 hour of theonset of signs and symptoms4if thecorrect diagnosis is not established.

Non-Rebreather Mask (NRB)

A face mask and reservoir bag device that delivers high concentrations of oxygen. The patient's exhaled air escapes through a valve and is not rebreathed.

Ventilation-Perfusion Ratio (VQ)

A normal ventilation/perfusion ratio is reported as 1:1. V is for Alveoli ventilation Q is for exchange at capillary membrane The volume of blood perfusing the lungs each 1 min is 4-5 L, and is approximately equal to the volume of gas that reaches the alveoli each minute (4-5 L). In a perfect match the portion of lung would receive 1 mL air (V= Ventilation) for each ml of blood flow (Q=perfusion) MEASURES ALVEOLAR PERFUSION V. SYSTEMIC BODY PERFUSION MEASURED BY MAP

ABGs in PE

ABG analysis is not diagnostic for PE but typically shows PaO2 <80 mmHg and PaCO2 < 36 mmHg on RA PaO2< 80 mm Hg and respiratory alkalosis Normal PaO2 does not exclude pulmonary embolism

Low VQ

Alveoli issue/BLOCKED VENTILATION - collapsed, blocked or filled with fluid Exs: COPD, pneumonia, asthma; Also caused by atelectasis, pain with breathing

Allergy Nursing Care and Pt Ed

Assess & document: •Allergy History •Assess for allergy response when giving new meds, especially antibiotics. Provide Patient /Family Ed •Avoid trigger •Practice on EpiPen. •Allergy ID tag. •Allergy testing follow up.

A 23yo patient develops sudden shortness of breath & dropping O2 pulse ox sat to 90% on 4LNC post-repair of a fractured pelvis and femur 4 days prior. In assessing, the RN knows the most probable cause of the respiratory distress is: A. Bronchitis B. Pulmonary Embolism C. Atelectasis D. Asthma Attack

B Sudden onset Immobile Fracture No mention of wheezing Bronchitis would be a cough Atelectasis takes longer to develop.

CPAP

Because CPAP only delivers one pressure setting it is important to understand that it helps best in situations of hypoxemia as it will aid with oxygenation. CPAP will do the following: ↑O2 ↓ Work of breathing ↑ Intrathoracic Pressure which will ↓ preload thereby ↓ cardiac workload Due to these effects of CPAP it can be useful in situations of sleep apnea and CHF exacerbation. The only real settings for CPAP that the nurse needs to keep in mind is the initial pressure setting . . . measured in cmH2O. Remember . . . CPAP is spontaneous . . . which means the patient does not receive any ventilatory support. If you have a patient whose ABG shows "normal" acid-base/CO2, but hypoxemia (that is refractory to increased FiO2) then CPAP might be a good place to go.

Ativan

Benzodiazepine: calms patient by depresses respiratory drive; so it is contraindicated in patient with respiratory issues.

BiPAP

BiPAP is a great tool for ventilation (removal of CO2) in conditions like COPD exacerbation or other situations where the patient needs ventilation support. Settings for BiPAP written by the physician will look like this: Bipap 10/5 rate of 12 FiO2 of 60% Notice the two pressures (IPAP vs EPAP). The difference between these two numbers is called PRESSURE SUPPORT. In the order above PS is 5 . . . IPAP - EPAP or 10-5. Notice also that they physician has ordered a RATE. This is a big difference between BiPAP and CPAP. With BiPAP a specific rate is programmed in the machine and whether or not the patient is breathing, the machine will deliver the programmed pressure at the set rate. Also, notice the order has a set FiO2 . . . this is the % of O2 to be delivered. Normal room air has an FiO2 of about 21%. The FiO2 will be titrated to keep the patients SpO2 (pulse ox) or SaO2 (blood gas) at or above 91%. If the patient continues to have difficulty maintaining appropriate SpO2 or SaO2 . . . the FiO2 can be adjusted. If CO2 levels are high then IPAP and EPAP can be adjusted accordingly. As Pressure Support increases (difference between IPAP and EPAP) the lungs will be able to expand more to allow increased ventilation (clearing of CO2).

High VQ

Blood Flow Issue Exs: pulmonary embolism, hypovolemia

Asthma Rx

Bronchodilators (Albuterol, Porvental, Xopenex) Anticholentergic (Atrovent (Ipratropium) to decrease mucous Mast cell stabilizers for long term treatment to prevent release of histamine Leukotrienne modifiers (singulair)

Resp Failure Type 2

CO2 not getting out Hypercapnia Pt not doing deep enough breathing ex: bronchitis - hard to exhale with mucous in bronchioles

Hypoxemia S/S

Changes in LOC if older ↑ HR ↑ RR - MOST IMP S/S Dyspnea Agitation ↑ WOB BE CAREFUL w/older ple: they can be on beta blockers, which hides ↑ HR

Chem 20

Chem 14, PLUS additional tests: D Bili Phos Uric GGT LDH Chol

Chem 14

Chem 8 + Albumin Total Protein ALP - liver tests ALT ASP Bilirubin Comprehensive Metabolic Panel (CMP)

Chest Xray's Role in PE

Chest radiographs are not diagnostic for pulmonary embolism but may rule out diseases that may mimic pulmonary embolism. Pleural effusions are noted in 48% of patients with pulmonary embolism. The Westermark sign, the Hampton hump, and pleural effusionin pulmonary embolismRule out other causes of dyspnea

Massive PE

Complete blockage of one or both of major pulmonary arteries losing more than 50% of the lung volume A whole section of a lobe can be taken out with massive

Anaphylaxis Management

Document allergy hx conduct more allergy tests Assess for allergic response w/ new meds Educate pt & family (notify primary care doctor of new allergy, use an allergy bracelet keep an epipen ON YOUR PERSON* No CXR necessary

Tissue hypoxia

Effects are multi-system •Cardiovascular •Tachycardia •Hypertension •Dysrhythmias Polycythemia Respiratory •Tachypnea •Hypoxemia (blood gas reading) •Cyanosis Neurological •Anxiety & agitation •Confusion •Headache •Weakness & drowsiness •Double vision •Impaired judgment •Coma

Asthma S/S

End Expiration wheezes when trying to force air out Otherwise the patient can have have oxygen trapping and inability to get adequate inhaled volumes

3 concentrations of epinephrine

Epi Pen: 0.5mg Epi IM/SQ: 1:1000 (1mg/mL) - not given rapid or IVP Epi IVP - 1:10,000 (0.1mg/mL)

Shunt

Extreme VQ Mismatch Blood goes back to heart without participating in gas exchange; large number of alveoli are blocked, filled with fluid, or damaged OR there are blood clots blocking the vascular system - 50% of the blood is going from the right to the left without getting properly oxygenated....common in acute respiratory injury through COVID - can cause death from COVID To compensate for a blocked area, in the pulmonary blood vessels your body will actually VASOCONSTRICT blood vessels in the area of the where there is a problem and try to move the blood to areas of the lung that have good V/Q matching. Intrapulmonary shunt is most common: alveoli filled with fluid: Clinical conditions: severe infection, advancing COPD, or Pulmonary Edema Anatomic shunt: ventricular/septal defect) bypasses lungs all together; congenital defect.

Allergy S/S

Facial & tongue edema Use of accessory muscles Throat Clearing Tripod position Wheezes bilaterally Worried/anxious facial expression SOB Itchy throat

Nursing Interventions to Optimize Oxygenation

Give O2 Position HOB Clear secretions Monitor O2 sat Notify Rapid Response & MD Frequent re-assessment Reverse narcotics/sedatives prn Tests: ABG, Chest X-ray, CBC •Low O2 = Aggressive O2 therapy •High CO2 = Increase rate and depth of breathing (Get patients out and moving.)

Hypercapnia

High CO2 •Can not get CO2 out of bloodstream •Pulmonary structures/CNS/NeurMusc ususally seen together with hypoxia, ususally we first see hypoxia and then hypercapnia Exs of Hypercapnia: - Airways/Alveoli = COPD - airflow obstruction and air trapping = asthma/cystic fibrosis - CNS = opioid overdose, brain stem stroke interfering with respiratory drive - Neuro/Muscular = MS, muscular dystrophy, Guillain-Barre

Helical (Spiral) CT

High accuracy for detection of emboli in main or lobar pulmonary arteries In one breath hold, the tube can go all the way around the patient and get a scan.

Allergy to Anaphylaxis S/S

Hives swelling (tongue and face edema) itching bronchial constriction (wheezes/stridor) difficulty breathing rapid RR/shallow breaths increased HR dropping BP circulatory collapse due to overwhelming inflammatory response

PE Risk Factors

Hx DVT/PE, Known DVT, Recent surgery, Immobilization, A-Fib, Cancer, Pregnancy/Birth Control Age Recent surgery Prolonged immobility Cancer Female sex (due to OB status and BC hormonal tx) Pregnancy Polycythemia Sickle cell anemia Genetic or acquired thrombophilia Obesity Trauma Burns Cardiac disease/congestive heart failure Previous deep venous thrombosis or pulmonary embolism Any abdominal or thoracic surgery lasting more than 30 minutes increases the risk of development of venous thromboembolism. PE is 10 times more likely to develop in pregnant and postpartum women than in nonpregnant women. Smoking, pre-eclampsia, and delivery by cesarean section are reported to increase pregnancy-related risk of venous thromboembolism. The expanding uterus obstructs venous blood return, posing increased risk for thrombus formation in the venous system of the pelvis or lower extremities.

Allergy

Hyperimmune response to an antigen; Mast cells and basophils release histamine mediated by IgE Antigen: any foreign particle, usually a protein (food, environmental, vaccines, insects)

Acute Respiratory Failure

Inability of the body to meet tissue O2 need &/or CO2 removal MUST LOOK AT ABGs on room air: PaO2 < 50mm Hg (ref 80-100mmHg) or PaCO2 > 50mm Hg (ref 35-45 mmHg)

Moderate Risk Pt Tx for PE

LMWH or low dose unfractionated heparin

Arterial Hypoxemia

LOW PaO2 r/t ALVEOLAR HYPOVENTILATION Lower than normal amount of oxygen dissolved in plasma (blood) Decreased O2 available for the RBC to pick up and carry problem with the alveoli capillary membrane thickening or fibrosis of the membrane happens with disease processes like cystic fibrosis, or ARDS. other common causes are neurological injury or drug overdose.

Anaphylaxis S/S

Low BP Throat tightness No response to first round of meds Tongue swelling Inspiratory stridor Rapid RR Increasing HR Shallow breaths Hives Mouth/throat itching Clearing throat/cough Difficulty breathing/wheezing

Hypoxia

Low oxygen saturation not enough O2 in the bloodstream alceolar/capillary membrane issue Exs of hypoxia: Pulmonary edema, ARDS, Drowning, Pulmonary Embolism, lung tumors

Hypoxemia PaO2 Ratings

Mild: 60-80 mmHg Moderate: 50-60 mmHg Severe: <50 mmHg Life Threatening: < 40 mmHg ALWAYS EVALUATE THE PAO2 FIRST

BiPAP (bilevel positive airway pressure)

Non-Invasive Ventilatory Support Positive airway pressure of inspiration and expiration (but higher on inspiration) + FiO2 If you have trouble breathing, a BiPap machine can help push air into your lungs. You wear a mask or nasal plugs that are connected to the ventilator. The machine supplies pressurized air into your airways. It is called "positive pressure ventilation" because the device helps open your lungs with this air pressure. Similar to mixing pressure support ventilation with CPAP Issues: Anxiety, Eating, Coughing Acts as a bridge for Respiratory Distress to try for up to 48 hours to avoid intubation; especially on people with COPD because they quickly become ventilator dependent and are hard to wean off the vent. Don't want them eating or drinking at this point All the pressure can cause bloating or vomiting....IV hydration offered only Challenging if pt needs to cough

Continuum of Respiratory Distress

Normal --> Distress --> Failure --> Arrest aeb: ↑ Work of breathing ↑ HR ↑RR ↑Use of accessory muscles Tripod position Nasal flaring Unable to speak in full sentences Lung sounds

PAO2/FIO2 RATIO MATH

Normal: PaO2 80-100 on an FiO2 of 21%. The P/F ratio distinguishes among mild (<300), moderate (<200), and severe (<100) ARDS Look at the ABG to find the PaO2 and the FiO2 (fraction of inspired oxygen) the pat was on when the ABG was drawn. --> For example: PaO2 on room air which has 21% FiO2 (converts from % to decimal to be 0.21) Ex: PaO2 85/FiO2 0.21 = 404 normal ratio finding Ex: PaO2 65/FIO2 0.21 = 309 Pt with COPD that lives with mild hypoxemia; SOB with activity Ex: PaO2 60/FiO2 0.28 (2LNC for SOB) = 214 meets criteria for acute lung injury; early respiratory distress; evaluate other symptoms VO's ratio: PaO2 69/FiO2 0.8 (on non rebreather??) = 86 severe acute lung injury; will correlate with symptoms of late acute respiratory failure pending respiratory arrest given the high level of FiO2 already

Resp Failure Type 1

O2 hypoxia

EARLY SIGNS of Acute Respiratory Failure

PaO2/FiO2 ratio 300-350 - restlessness, change in LOC - WOB increased - RR/HR increased - normal or abnormal lung sounds - dyspnea - SpO2 decreased - PaCO2 decreased (resp alkalosis) - decreased PaO2 - possibly patchy white infiltrates on chest xray

Thoracic trauma

Penetrating or blunt CT used to assess both kinds

Thoracentesis Nursing Responsibilities

Pre: Consent signed; patent IV access; place on NC oxygen as needed or have available, check room safety for oxygen/AMBU bag with face mask/working suction; Position the patient sitting upright to enable the pooling of the fluid in the bottom of the lung, leaning over a bedside table is preferred, patient must hold still, pre-medicate for pain, place on EKG monitor and continuous pulse oximetry monitoring, oxygen as needed. During: monitor VS, O2 sat, cardiac rhythm, pain level and give additional meds as ordered Post: Continue to assess VS and breathing, obtain chest X-ray, monitor needle insertion site for bleeding and crepitus.

Aortography in PE

Reference standard test Allows direct visualization of pulmonary vasculature to identify areas of obstruction

Tissue Hypoxia - low urinary output

Renal: low urinary output Urine Output is an excellent indicator of tissue perfusion. The kidneys receive 25% of the cardiac output, so if there is a lack of tissue perfusion the kidneys reflect that and the urine output is decreased. This is why we do I &O , and why in the ICU we do it hourly.

ECG Results in PE

Rule out myocardial infarction, aortic dissection Anterior T-wave inversion common in pulmonary embolism Strain pattern in right side of heart (S wave in lead I, Q wave in lead III, T-wave inversion in lead III), new right bundle branch block, and right-axis deviation seen in pulmonary embolism Anterior T-wave inversion is evident in 85% of cases of PE. This abnormality reflects inferoposterior ischemia that results from pressure overload. Tall peaked P waves ,tachycardia, new incomplete right bundle branch block, and right-axis deviation are the most common abnormalities noted in patients with pulmonary embolism.

Vasopressor

Rx to increase MAP in cases of ARDS or Sepsis THINK VASOCONSTRICTION drug that constricts or narrows the diameter of a blood vessel The major vasopressors include phenylephrine, norepinephrine, epinephrine, and vasopressin.

PE s/s

SUDDEN ONSET The "classic" signs and symptoms of pulmonary embolism, namely tachypnea, dyspnea, hemoptysis, apprehension, and chest pain, occur in fewer than 20% of patients. Acute-onset dyspnea and tachypnea are the most common initial s/s, and patients often report a feeling of apprehension. symptoms of right-sided heart failure. JVD, increased central venous pressure, tachycardia, tachypnea, hypotension, a new murmur due to tricuspid regurgitation, and decreased SpO2

Acute PE

Scattered - clot shatters and starts to go up smaller branches

Epinephrine (Adrenaline)

Secreted by the adrenal medulla; increases heart rate and blood pressure and dilates airways (sympathomimetic). It is part of the body's "fight or flight" reaction. Epinephrine, more commonly known as adrenaline, is a hormone secreted by the medulla of the adrenal glands. Strong emotions such as fear or anger cause epinephrine to be released into the bloodstream, which causes an increase in heart rate, muscle strength, blood pressure, and sugar metabolism.

Low Risk Pt Tx for PE

TEDS, SCDs

Difference b/w BiPAP and CPAP

The major difference to keep in mind between these two is that CPAP is delivering a set pressure CONTINUOUSLY . . . it never changes. It doesn't matter how fast the patient breaths, whether they are taking a breath, or if they stop breathing . . . it will just keep pumping along at the same pressure. Bilevel on the other hand is much more sophisticated. BiPAP will deliver a DIFFERENT pressure depending on whether the patient is taking a breath or exhaling.

Calculate the partial pressure of oxygen in arterial blood (PaO2) to fractional inspired oxygen concentration (FiO2) (PaO2/FiO2 or P/F) ratio for a patient with possible acute respiratory distress syndrome (ARDS) who has PaO2 of 60 mm Hg while receiving FiO2 of 80%. Record your answer using a whole number. _________

The patient's PaO2/FiO2 is 75, based on the PaO2 to FiO2 equation: 60/0.80 = 75.

PEEP

The same as CPAP... just on a vent!

Saddle Embolism

Thrombus that occludes thebifurcation of the pulmonary arteryis termed a saddle embolus straddles bifurcation of a vessel and blocks, e.g. sits on 2 main subdivisions of pulmonary artery

Chest Tube

Tx for pneumothorax if lung volume loss > 20% •Remove air or fluid from pleural space •Re-expand the lung top tube over 2nd rib: air removal bottom tube over 5th rib: fluid/blood removal

VQ mismatch "shunt" in VO's case

Vent/Perfusion Imbalance COPD, asthma, atelectasis, emphysema, hypoventilation, pulm edema, pulm embolism, aspiration pna

Medical Tx for PE

Volume resuscitation Administration of vasopressors Anticoagulation Administration of thrombolytics

Dry Suction Chest Drainage Unit

WAY MORE COMMON Atrium Oasis Most commonly dialed to -20 for adults; -10 for peds Taken out a full lung can be up to -30 Bellows comes out to arrow piece Drainage, air leak, suction source (only 3 chambers) Turn unit on to suction if bellows is not showing....

Pulmonary Embolism Patho

Whenthe embolus lodges in the pulmonary vasculature, blood flow to the alveoli beyond the blockage is eliminated. The obstruction causes a section of lung to be ventilated but not perfused, thus creating intrapulmonary "deadspace." The blockage acts like a dam, causing blood pressure to increase in the vessels upstream. The right ventricle must then generate tremendous pressure to overcome this obstacle and maintain forward blood flow and perfusion to distal organs. If the right ventricle is unable to maintain adequate forward blood flow, right-sided heart failure develops and leads to hypoxemia, dyspnea, hypotension, and syncope. In a massive pulmonary embolism, cardiac arrest occurs because the left ventricle is unable to maintain adequate cardiac output.7Pulseless electrical activity is the most common rhythm seen in cardiac arrest. Only 25% of patients with cardiac arrest survive the ordeal, and a preoperative cardiac arrest is the strongest predictor of postoperative mortality.

Tension Pneumothorax

a pneumothorax with rapid accumulation of air in the pleural space causing severely high intrapleural pressures with resultant tension on the heart and great vessels. heart moves over and trachea

Ventilation-Perfusion scan

a scan that tests whether a problem in the lungs is caused by airflow (ventilation) or blood flow (perfusion) A low or indeterminate result does not eliminate diagnosisof pulmonary embolism

Cyanosis

a very late stage of RF

Pore of Kohn

allows for communication of air between alveoli in the event one of them collapses (e.g., mucous plug) if we get our patients to deep breath, cough move, use the IS they can actually recruit adjacent alveoli USE "IS" normal tidal volume: quietly talking about 500-700, big breaths sh/be 1000-1200.

If increasing agitation and dys-LOC, get...

an ABG not a pulse ox SpO2 tells us nothing about PaO2 and Pa CO2

Biggest concern w/ thoracic trauma

atelectasis

Chem 7/8

blood measurements of: BUN, Cr, BG, Ca+, CO2, Cl-, Na, K+ Basic Metabolic Panel (BMP) - usually contains 8 tests, all of which are found in the CMP (below). It provides information about the current health of your kidneys and respiratory system as well as electrolyte and acid/base balance and level of blood glucose

With respiratory concerns you always need to also work up....

cardiac tissue hypoxia could be due to "pump" issues, not just ARDS

If pt has a suspected PE....

don't get them up and moving oxygenate them

Echocardiography (ECHO) in PE

echoes generated by high-frequency sound waves produce images of the heart New severe tricuspid regurgitation and pressure overload in right ventricle in pulmonary embolism Transthoracic echocardiography for detection of intra-cardiac thrombi Transesophageal echocardiography for detection of thrombi in central pulmonary artery

Polycythemia

effect of tissue hypoxia A disorder characterized by an abnormal increase in the number of red blood cells in the blood SIRS process can stimulate the clotting cascade

D-Dimer Lab Test

elevated when you have too much clotting everywhere 90% negative predictive value if <500 mg/L The D-dimer assay is a sensitive but nonspecific test to detect the presence of venous thromboem-bolism. D-dimers are produced during the degradation of fibrin clot by plasmin. The D-dimer level may be elevated in other conditions, such as infection, cancer, pregnancy, surgery, renal failure, or heart failure. D-dimer assay has a negative predictive value of 90% when results are <500mg/L. In essence, the nurse is virtually assured that pulmonary embolism is excluded from the list of possible diagnoses when the D-dimer level is < 500mg/L. recent pregnancy elevates D-dimer levels

Pulmonary Embolectomy

excision of a pulmonary embolism Seven world cases ofsuccessful survival after postcesareanpulmonary embolectomy have beenreported worldwide, and only 2 ofthose patients survived without per-manent neurological damage

Most common cause of thoracic trauma

fractured ribs

The nurse is caring for a patient with 2 chest tubes on the right that are "Y'd" to 1 "wet" chest drainage unit. There is bubbling in the suction control chamber. The nurse knows this indicates: A. The patient has an air leak. B. Chest tube is to water seal drainage. C. The chest tube is to suction. D. The lung is fully expanded.

if it was to water seal drainage, there would be no bubbling....that would be a gravity situation A wet suction unit has a water level that determines the level of suction. Bubbling in the suction control chamber indicates that the chest tube is to suction, not water seal. To assess the suction level on a "wet" chest drainage system, momentarily take the patient off suction and assess the water level, add or subtract fluid as needed to maintain the right level.

WOB

look at the sternocleidomastoid muscles at side of neck, they fair, also look at chest with clothing off to assess intercostal muscle retraction) - staccato speech Expiratory "grunt' sound is also their attempt to keep alveoli open longer by slowing down expiration

High Risk Pt Tx for PE

low molecular weight heparin

Nursing care of chest tubes

make sure: - no air leaks - water level in wet sxn unit has not evaporated/decreased - for adults typically 20 cm - have to temporarily remove it from sxn to check - initially no more than 100mL/h of bright red blood

For pt progressing along the Resp distress continuum, nursing actions would be....

more O2 - OxyMask/HFNC, CPAP might come later HOB elevated Rapid response call Charge nurse call - offload some other pts As a primary response, you stay with your pt who is having problems; hand more stable pts on to others Another chest xray/ABGs/H&H Will request RT and the MD and rapid reponse

Timeline of Hypoxemia and Hypercapnia

most commonly occur together in RD/RF •PaO2 decreases first à--> •Causes drive for more O2 --> •RR/HR increases --> •Initially drops PaCO2 levels --> •Patient tires and CO2 levels increase RESULT: Low PaO2 & High PaCO2

Wet Closed Chest Drainage System

the use of a chest tube and closed drainage system to re-expand the lung and to remove excess air, fluid, and blood Amount of sxn on the wall doesn't determine the sxn, instead it is the "cm" of water..... can either be connected to sxn source (water or wall depending on system) or "to gravity" letting gravity drain air and fluid

Massive Pulmonary Embolism

thrombus occluding more than 50% of the pulmonary vasculature.

Thoracentesis

tx/dx for pleural effusion used for situations in which the effusion is small, affecting < 25% lung volume and pt is not unstable clinically a surgical perforation of the chest wall and pleural space with a needle to obtain specimens for diagnostic evaluation, to instill medication into the pleural space, and for the removal of air and fluid form the pleural space.

Virchow's Triad

venous stasis, hyper-coagulability, and vessel wall damage triggers a venous thrombus(clot)

LATE SIGNS of Acute Respiratory Failure

•Agitation --> lethargy --> unresponsiveness •VS: RR, HR, ¯BP •Severe WOB: grunting, retractions, cyanosis, pale mottled skin •Lungs: crackles, rhonchi, diminished BS ABG: •decreasing PaO2 (despite increasing levels of FiO2) •Acidosis (Ph <7.35) Chest X-ray: Bilateral Infiltrates "White Out"

Pulmonary Contusion TX

•Careful respiratory assessment •Pain relief Oxygen therapy

Pulmonary Contusion

•Damaged lung parenchyma - impaired gas exchange •Interstitial hemorrhage, alveolar collapse, and alveolar flooding •Continued perfusion of unventilated lung portions ® shunting and hypoxia

PE Effects

•Distal blood flow eliminated •¯ lung compliance •¯ surfactant results in unequal gas distribution, WOB, and stiffened alveoli Pulmonary hypertension

PE Dx

•Does patient have risk factors? •ABG analysis •Low O2 •Initial low PaCO2 - increasing PaCO2 •Doppler ultrasound: Presence of DVT •Spiral CT •V/Q scan (older test, not as valid) Pulmonary angiogram in IR

Pulmonary Contusion s/s

•Dyspnea •Wheezing hypoxia •Hemoptysis •Cyanosis - Bloody sputum

Anaphylaxis Rx

•Epinephrine (SQ or IM) 1:1000; given immediately with first s/s •Antihistamine (IV or PO) - ex diphenhydramine (Benadryl) 50 mg IVP or oral of rxn is mild •Breathing treatment (NEB w/albuterol or possible atrovent) •Glucocorticosteroids (IV) •IV Fluids (Normal Saline)

Hypercapnia S/S

•Lethargy •Decreased LOC •Decreased RR •Low Tidal Volume (shallow breaths) CO2 is a respiratory acid....acid drops the pH Acidosis leads to signs of lethargy and s/s above.... Acids are much more detrimental than alkalotic states Sepsis is a lactic acidosis DKA is a metabolic acidosis

PE Etiology

•Venous stasis: Obesity, immobility, LL paralysis •Altered coagulation: Cancer, arterial fibrillation, hx DVT •Vessel damage: Trauma, bone fractures, sepsis, atherosclerosis, orthopedic surgery (50%), general surgery (30%) Cancer pts at VERY HIGH RISK Need anticoag meds SCDs Decreased lung compliance Decreased surfactant