Respiratory Part 1 Flashcards
Acid-Base Balance
The process of regulatingthe pH, bicarbonateconcentration, and partialpressure of carbon dioxideof the body fluids
Regulated through respiratory and renal functions
Gas Exchange
oxygen is transported to the cells and carbon dioxide is transported from the cells
Perfusion
flow of blood through arteries and capillaries delivering nutrients and oxygen to cells and removing cellular wastes
Upper Respiratory Tract anatomy
Nasopharynx
Oropharynx
Laryngopharynx
Lower Respiratory Tract anatomy
Bronchioles (Trachea)
R and L lung
- alveolar ducts
- alveoli
What the different airway obstructions?
- blockage from alveolar compromise (Pulmonaryedema)
- collapsed lungs (Atelectasis)
Pulmonary edema (cardiogenic) caused by
backup of fluid that the heart cannot clear
Non-cardiogenic PE caused by
inflammation from injury and/or infection
ARDS (trauma to the lungs causing redness and swelling)
Atelectasis is caused by
collection of air or blood outside the lung but within the pleural cavity - a portion of the lung collapses
- Pneumothorax
- Hemothorax
Pulmonary embolism occurs when
blood clot that is lodged in a blood vessel in the lungs blocking blood flow to part of the lung.
- Surgical pts, clotting disorders prone
Perfusion obstruction includes
pulmonary embolism
Tidal volume
the volume of air exchanged with each breath
6-8mL/kg is approximately what in mL of tidal volume
400-500
FiO2 is
fraction of % of inspired O2
RA FiO2
21%
Nasal Cannula 4-6L FiO2
37-45%
High Flow 60L/min FiO2
100%
MAP normal
> 65 mmHg (perfuse organs)
If the MAP is extremely high, what is happening
no perfusion
- no cap refill, mottling
What is the formula for MAP?
SBP + 2 (DBP) / 3
MAP shows
how much Oxygen is being perfused in the tissues
ABGs is used to
maintain homeostasis
- Respiratory CO2
- Metabolic HCO3
pH normal
7.35-7.45
< 7.35 pH
acidic
> 7.45 pH
alkalosis
PaO2 normal
80-100 (how much O2 is in arterial blood)
SaO2 normal
> 95%
PaCO2 normal
35-45 mmHg
<35 PaCO2
hypercapnic
> 45 PaCO2
hypercapnic (retaining too much
HCO3 normal
22-26
CO2 is the
ACID component of our blood
- lungs regulate the CO2 levels within minutes
To compensate for acidosis
RR and depth will increase to blow off CO2
To compensate for alkalosis
the RR and depth will decrease to retain CO2
PaO2/FiO2 Ratio is used to determine
determine lung injury
Normal Lung ratio
300-500
Acute lung injury ratio:
200-300
ARDS: < 200
very significant injury
ARDS: <100
severe injury with high mortality
Acute lung injury is like ARDS but has
less of a shunt resulting in hypoxemia
Normal lungs require
little outside O2 to maintain a normal PaO2
- 21%
As lungs become injured, they require
higher concentrations of supplemental O2
Lung injury formula
PaO2 (arterial O2) divided by FiO2 (oxygen %)
V/Q is the
ventilation to perfusion ratio
(V)
air moving in & out of the lung
- bringing oxygen in to /removing CO2 from the alveoli
(Q)
blood circulating to areas of the lung
- removing O2 from the alveoli and adding CO2 so the Co2 can be blown off by the lungs
In the lungs normally, V and Q are
the volume of blood perfusing the lungs and the amount of gas reaching the alveoli are almost identical
Why is the V/Q ratio important?
the ratio between the ventilation and the perfusion is one of the major factors affecting the alveolar (and therefore arterial) levels of oxygen and carbon dioxide
If the V and Q are imbalanced, the patient will develop
hypoxemia on RA
- providing O2 will correct until the true cause can be addressed
A clot in the vascular or perfusion side prevents blood from circulating effectively in the pulmonary capillary in that area where some of the alveoli are, so even if the alveoli bring in O2 the blood stream cannot pick it up in that area – it is a _________ issue.
perfusion
If pneumonia secretions are sitting in the alveoli preventing breathed in oxygen to reach the pulmonary capillary of those alveoli the blood rushes by but is unable to pick up oxygen in that area – it is a ____________ issue.
These situations create a VQ mismatch and in these cases cause a respiratory failure event.
ventilation
Hypoxemia Respiratory Failure
decreased O2 gas exchange
- V/Q mismatch or impaired diffusion at alveolar level
- ventilation or perfusion failure
Early hypoxemia PaO2
<80
Late hypoxemia PaO2
<60
Hypoxemia leads to
Inadequate alveolar ventilation causing hypoventilation
Inadequate alveolar ventilation causing hypoventilation
- alveolar blockage
- perfusion blockage
- airway obstruction
- respiratory depression
Alveolar blockage includes
pulmonary edema
pneumonia
ARDS
cystic fibrosis
Perfusion blockage
pulmonary embolism
Airway obstruction
Asthma
COPD
Anaphylaxis
Atelectasis
Bronchospasm
Respiratory depression
opioids overdose
Hypercapnia
decreased CO2 removal
- causes ventilation failure
Late hypercapnia PaCO2
> 50
Early hypercapnia PaCO2
> 45
Hypercapnia can lead to
inadequate alveolar ventilation causes hypoventilation and CO2 retention
Hypoventilation and CO2 retention caused by
- CNS (spinal cord injury and opioid overdose)
- Neuromuscular (MS and ALS)
- Barrel chest, kyphosis, trauma - open thorax wound
- COPD and Cystic fibrosis
Hypoxia is the 1stsign of
hypoxemia …
Hypoxia is the
reduction of O2 at the tissue level (SaO2)
Hypoxemia is the
reduction of arterial oxygen tension or partial pressure of oxygen PaO2
S/S of hypoxemia respiratory failure
Dyspnea
Tachypnea & tachycardia
Coughing
Wheezing
Confusion
Cyanosis (Bluish/purplish) color in skin, fingernails, and lips
Hypercapnic respiratory failure is also known as
ventilatory failure
- decreased ventilation or CO2 removal
COPD patients typically have a higher rate of
CO2
S/S of Hypercapnic
Hypoventilation (dyspnea) – unable to remove CO2 from body
Tachycardia
Diaphoresis
Headache
Restlessness
Change in consciousness – CO2 sedates – so very lethargic
Consequences of hypercapnia
slow changes in CO2 allow for compensation (tolerate high CO2 better than low O2)
- TX PRIMARY CAUSE BEFORE THEY DETERIORATE
When CO2 levels cannot be maintained within normal limits by the respiratory system, one of two primary problems exists:
(1) an increase in CO2 production
(2) a decrease in alveolar ventilation.
Hypoventilation caused by
Blockage in alveoli
Airway obstruction
Perfusion blockage
Issues with mechanical movement of thorax
What happens in hypoxemia or hypercapnia?
Diffusion limitation
Shunting
Alveolar hypoventilation
Shunting
blood exits the heart without taking part in gas exchange as this is a perfusion issue:
- i.e. cardiac-like septal defect, cardiogenic pulmonary edema
- PE is not going to be perfused
Diffusion limitation occurs when
gas exchange across the alveolar-capillary membrane is compromised by either the destruction of the alveoli or blockage within the pulmonary capillaries
SO EITHER PERFUSION AND/OR VENT ISSUES: i.e., ARDS, pulmonary edema
Alveolar hypoventilation
decrease in ventilation that causes hypercapnia and hypoxemia which is typically caused by vent issues:
- i.e. CNS conditions, acute asthma, chest wall dysfunction (respiratory paralysis, flail chest)
S/S of early respiratory failure
mental status changes (confusion)
dyspnea
tachypnea
tachycardia
hypotension
refusal to take oral fluids
decreased urination (concentration)
wheezing
persistent cough
Late s/s of respiratory failure
bradycardia
bradypnea
increased CO2 HA morning, decreased LOC and RR
lethargic
unresponsive
cyanosis (PaO2 is < 45)
What does cyanosis look like in darker skin tones?
purple (lips, oral mucous, clubbing
pallor (hands, conjuctivia)
ARDS is
pulmonary edema due to trauma or infection
Causes of ARDS
Aspiration of gastric contents
Near drowning
MVC
Chemical Inhalation (paints etc.) – need to wear a mask
Sepsis
COVID-19
Viral pneumonia, fat emboli, decreased surfactant production, fluid overload, and shock
S/S of ARDS
Changes in LOC
Severe dyspnea and coughing
Tachypnea and shallow
Inspiratory crackles – Rice Krispies
Hypoxemia unresponsive to O2
Tachycardia
Cyanosis
Orthopnea – can’t breathe when lying down (sit them up)
increased WBC
respiratory distress
These s/s of ARDS cn lead to what intervention
- Profound dyspnea,
hypoxemia,
increased WOB
respiratory distress
endotracheal intubation
A chest x-ray of ARDS shows
white out and plural effusions
ARDS can lead to
severe hypoxemia
hypercapnia
metabolic acidosis
organ dysfunction
ARDS phases
Exudative
Proliferative
Fibrotic
ARDS Exudative phase
Cell injury and inflammation
Alveolar edema decreases ventilation > hypoventilation occurs
- Low PaO2 and elevated PaCO2
- Whiteout on chest xray
Respiratory failure
- Classic sign >refractory hypoxemia (PaO2 < 60 mmHg)
Assisted ventilation needed
ARDS Proliferative phase
Edema fluid resorption
Recovery phase
ARDS Fibrotic phase
Fibrosis of lungs
Ventilator dependent breathing
Nursing interventions for ARDS
Assess respiratory rate, depth, and vitals
Administer oxygen
Fowler’s position (45 degrees)
Mobility – passive ROM, TCDB, turn the whole body (turn on the good side (good lung) to cause secretions)
Restrict fluid intake (Daily wts and I&Os)
Breathing treatments (AIMS)
Administer diuretics and/or glucocorticoid steroids (Furosemide and K
Prepare for intubation and mechanical ventilation if the patient declines
What position should a patient with ARDS lay on
the good side to get rid of secretions
What respiratory secretions are Rx to ARDS patients?
AIMS
- 1st Albuterol
- Inhaled and IV steroids
Blood sugar does what on steroids
goes up
If K is low
dysrhythmias and muscle weakness
Atelectasis causes
Pneumos: VALI (Ventilator Induced Lung Injury) – high PEEP and/or Tidal Volumes on vents
Either: Trauma
– MVC, gunshot wound,
Pneumothorax
open/closed wound causing air to enter chest wall
Hemothorax
blood in the pleural space causing atelectasis
S/S of Atelectasis
Tachycardia
Hypotension
Tachypnea
Shallow breathing
Hypoxia
Chest pain
Tension Pneumo = tracheal deviation
Pneumothorax causes
blunt or penetrating chest injury, certain medical procedures (high tidal volumes on mechanical vents), or lung disease
VALI
(Ventilator Induced Lung Injury) caused by high PEEP levels and/or Tidal Volume too high on ventilator; car crash with rib fractures causing either pneumo and/or hemo.
PEEP
Positive End-Expiratory Pressure
On a dry suction chest tube, the orange bellow means
connection to suction
Dry chest tube suction
stays at the suction on the dial regardless of the suction on the wall
Bubbling in the wet chest tubes suction chamber intervention
nothing normal (expected)
The water seal chamber should not
constantly bubble
= air leak
If pneumothorax in the water seal chamber bubbles
occasionally okay not constant
on expiration
If the chest tube becomes dislodged then
place in sterile water and place a 3 sided dressing on the incision site
What type of pressure is the chest tube restoring
negative pressure with releasing air or blood
Pneumothorax chest tubes are placed in
upper portion
Hemothorax chest tubes are placed in
placed in the lower portion
Nurses should assess for what in atelectasis patients
- Absent breath sounds on the affected side
- Cyanosis
- Dyspnea
- Decreased chest expansion unilaterally
- Hypotension
- Sharp chest pain
- Subcutaneous emphysema – CO2 or air leaking into the skin causing crepitus (crackling) feeling in skin
- Tracheal deviation to the unaffected side with a tension pneumo
=Tension pneumos seen with closed pneumos from closed-chest wounds or mechanical ventilation
=Creates a “one way” valve which allows air out of the lung, but not out of the pleural space creating a tracheal deviation - Monitor skin around insertion site
- Keep patient moving by turning frequently
- Keep sterile gauze at the bedside to place over site if the tube becomes dislodged
Mobility for atelectasis patients
ROM
TCDB
Turn frequently
Care of chest tubes
Dislodged from patient
Sterile dressing over site, taped on 3 sides, andcall the physician immediately
System breaks
Insert tube into sterile water or saline
Milking, stripping or clamping
NOT recommended
The drainage chamber is marked each
shift for output
If the drainage chamber is full,
chnage out system with a new one
Miking, clamping, striping could cause increase of
pneumo or cause a pneumo if the patient has a hemo
What to do if chest tube becomes dislodged?
Cover the site with a sterile dressing, and tape on three sides (this allows air to escape and prevent tension pneumothorax) and notify physician immediately.
What do you do if the System breaks?
Insert the tube 1 inch into a bottle of sterile water or sterile normal saline and obtain a new system.
Milking or stripping tubing?
Not recommended anymore because it creates too much negative pressure (always follow hospital policies)
Clamping tubing?
Increase risk of patient developing a tension pneumothorax. Never do it without an order and follow hospital policies.
Wet system type of chest tube
suction control uses water for the pressure
Dry system type of chest tube
suction control has a bellow (orange) for the pressure.
If the patient has a pneumothorax, the drainage chamber will have
nothing to monitor
Wet system suction chamber
needs water to suction
- refill PRN to Rx pressure as it evaporates overtime
- continuous bubbling noted as expected in wet system
- connect to suction
Dry system suction chamber
connected to suction and the orange bellow needs to be seen in the suction control window.
- There is no water in the suction control chamber with a dry system
Water seal chamber (wet and dry)
continuous bubbling = leak in system
- normal for tidaling (water move up and down) with inspiration
How do you identify crepitus?
Palpate around chest tube insertion site
- air leaking under the skin
Pulmonary embolism
Embolus lodged within the pulmonary system
PE causes
DVT (common), cancer, fat emboli (trauma – pelvic fx)
PE s/s
Severe dyspnea, tachypnea
Hypoxemia unresponsive to oxygen therapy
Chest pain
Tachycardia, diaphoresis
Changes in mental status
Syncope
Cyanosis
Pallor
How do you dx PE?
D Dimer lab – elevated levels from proteins that break down blood clots
CT Scan (1st)
What drugs combined can cause DVT - PE?
Dextromethorphan (Niquil) contraindicated with antidepressants
- Straddle
PE nursing interventions
Assess respiratory rate, depth, and vitals (1st)
Elevate HOB
Oxygen
Heparin therapy (PT, black stools-GI and stomach)
Warfarin (takes several days)
Mobility - cautious (ROM, TCDB, frequent turning)
Nutrition - deficits, calories, tube feedings, oral eating
Teaching about anticoagulant therapy
Coumadin (Warfarin) needs to limit
Vitamin K (moderation)
- green leafy veggies
Everything involving respiratory nursing mgmt
Assessment (VS, lung sounds, rate and depth of breaths, work of breathing)
Positioning (HOB, aspiration = side-lying, unilateral/bilateral
O2 Therapy (PaO2 > 60, SaO2 >95%)
Dx (CBC = WBC, RBC, H&H, platelets, ABG (sedative - retaining too much CO2)
- Chest Xrays = infiltrations, confirm chest tube placements (Hemothorax if white at the bottom)
Pharmacologic therapy and reassessments
Nutritional therapy
Mobility
sleep
pt education
If the patient is on a ventilator, then the patient should be
prone to move secretions
ARDS has a fluid
restriction
COPD patients with CO2
rely on the hypoxic drive to breathe.
- chemoreceptors that recognize CO2 are less sensitive to Co2.
- lack of oxygen that causes them to breathe.
-too much oxygen, they might become severely hypoxic because their drive to breathe is high CO2 and not high O2 levels.
But remember, never withhold oxygen from a hypoxic patient
O2 Delegation
cannot be delegated to UAP unless it is already in place.
RNs must assess and evaluate the patient before delegation**
When should you start enteral feedings with a respiratory/ventilator?
within 48 hours to keep gut working
Verify OG or HG tube with
xray confirmation prior to using it
What type of diet will a repsiratory patient eat
high protein promote healing
Parenteral feedings are through a
central line
Turn the pateint every
2 hours if tolerated
ROM or PROM should be done
every shift
If the patient is not vented then encourage
ambulation (early)
Sleep deprivation decreases
healing
T/F: Paralytic patients can still hear
yes
Pt edu for patient with respiratory problems
Labs and what they mean – understand what they are for so you can pass this along to your patients and their families
Oral care for vented patients
Medications – what are they for? What side effects?
Mobility – Incentive spirometer, ambulation
Sleep – importance of rest
Respiratory Meds - Bronchodilators
Beta blockers (1st albuterol)
Anticholinergic (2nd Ipratropium)
Methylxanthines
BAM and SLaM
Respiratory Meds - Anti-inflammatory
Steroids (Beclomethasone and Flutaxaxone – inhaled steroids)
Leukotriene inhibitors –(Montelukast)
Mast Cell stabilizers
Beta 2 Agonist
Albuterol 1st line for ashtma attack
- dilate bronchodilators
- immediate action
What are the expected s/s of Beta 2 agonists?
wheezing to diminish and hearing clear breath sounds
Anticholinergics med type
(Ipratropium – 2nd)
What are the expected s/s of Anticholinergics
– dry mucous membranes, tachycardia, hot/dry skin
Methylxanthines MOA
Bronchodilator and stimulatory effects
- LONG TERM CONTROL OF ASHTMA
caffeine
1st and 2nd Ashtma attack meds
Albuterol – 1st line used for asthma attack
Ipatropium – 2nd line for asthma attack
How to take bronchodilators?
Shake it before you take it
Breathe out, then inhale puffs
2-4 puffs every 20 mins
Nebulizer Bronchodilators if not effective after
3 doses = call HCP
Which inhaler goes first?
Bronchodilator
steroid inhalers
Nebulizer Bronchodilators are effective if
decrease in RR and O2 sats increased >90%
Nebulizer bronchodilator side effects (expected)
Tachycardia, Tremors, and insomnia (feels like adrenaline rush)
Steroids med types
(Beclomethasone and Flutaxaxone – inhaled steroids)
Steroids onset
Slow onset so not used as first line for asthma attack.
Inhaled steroids
need to rinse mouth or perform oral care – DO NOT SWALLOW WATER - as these can cause thrush
- swish and spit
Inhaled steroids on BG
not affect blood sugar, only IV (prednisone) does
Leukotriene inhibitors med type
Montelukast
Leukotriene inhibitors onset
Slow onset (1-2 weeks) but opens airway
- not a rescue drug
What is expected with Leukotriene inhibitors?
cough, sore throat, fatigue, headache
Mast Cell Stabilizers onset
Acts fast but is not rescue inhaler
Take Mast Cell Stabilizers 15 minutes before
exercise to reduce exercise induced asthma
DO NOT USE _______________ or _____________ as a primary for an asthma attack.
Salmeterol or Fluticasone
- long term inflammatory control of the bronchioles
How do I know if respiratory drugs are working?
Lung sounds, go down on FiO2 and stats go up, regular, rate
After an inhaled steroid on a ventilator patient, what needs to be done?
oral care
What diuretics could help respiratory illnesses?
furosemide, hydrochlorothiazide, bumetanide
spironolactone
What anticoagulants could help respiratory illnesses?
Injection: heparin, enoxaparin
Oral: warfarin, apixaban, rivaroxaban
What anti-inflammatory steroids could help respiratory illnesses?
Oral: prednisone
Oral or injection: methylprednisolone, dexamethasone, betamethasone
Inhaled: beclomethasone, fluticasone
Diuretics decrease
BP, decrease fluid (causing increased urination), and dehydrate
Furosemide or HCTZ: potassium
wasting
Spironolactone potassium
sparing
Nutrition education for Furosemide and HCTZ
encourage high potassium foods
Bananas, Oranges, Green leafy vegetables, Liver, avocado
Hypokalemia ECG
> flat T waves, prolonged QT, ST depression, U waves
ICU patients K needs to be
4-5
Spirinolactone nutrition
avoid K
Hyperkalemia ECG
peaked T waves, maybe ST elevation, P wave
Hyperkalemia KILLS
Anticoagulants do what
decrease the body’s ability to clot and prevent clots from forming allowing the body time to reabsorb and break down clots in the body already. They do not break down clots
**prevnt forming new clots and growth of existing clots
Heparins MONITOR
platelets (do not give if less than 100,000 mcL
Heparin Labs
PTT 46-70
Antidote for Heparin
Protamine Sulfate
Actions if PTT >70 or signs of bleeding from Heparin
STOP the heparin gtt and notify provider
Prepare antidote
Reassess labs in 1 hour
Warfarin Labs
INR levels for warfarin- therapeutic levels 2-3
Antidote for Warfarin
Vitamin K
Actions if INR > 4 in Warfarin
Assess for bleeding
Prepare Vitamin K
Actions if INR > 2 in Warfarin
Give warfarin to increase INR to 2.5
Which anti-coagulant is fast acting?
Heparin
Which anti-coagulant is slow-acting?
Warfarin
- 5 days therapeutic levels
PE patients in the hospital should be started on
Warfarin
- unless apixaban is Rx
Apixaban and rivaroxaban begin working within
few hours of taking so they can start after the heparin therapy. Can start on discharge. Does not require INR testing.
Nutrition education for anticoagulants
consistent levels of leafy green vegetables or liver which are high in Vitamin K. They do not have to avoid these but keep it in moderation.
ASA and clopidogrel
antiplatelets
Glucocorticoids used to
suppress immune responses like inflammation.
Prednisone and prednisolone are intermediate acting and have a half life up
36 hours
Dexamethasone and betamethasone are longer acting and have a half life up to
50 hours
Which glucocorticoid is only give orally?
prednisone
Side effects of Glucocortoids
Hyperglycemia, infection, insomnia, polydipsia, polyphagia
- No need to report to HCP as this is an expected finding, but should be part of patient teaching
Hypokalemia can occur with what interaction cobination: glucocorticoid and
HCTZ and loop diuretics
Glucocorticoids can cause insomnia so take
early in the day
Patient with severe asthma presents to the ER with the following vital signs: HR 120 BPM, RR 32 BPM, O2 Sat 90% on room air and a Peak Expiratory flow of <40%. What medication would you give? Select all that apply
- Inhaled salmeterol
- Albuterol inhaler
- Nebulizer ipratropium
- IV Methamphetamines
- IV Methylprednisolone
- Albuterol inhaler
- Nebulizer ipratropium
- IV Methylprednisolone
Think AIM – albuterol, ipratropium, steroid
BAM and SLaM
The emergency department nurse is assessing a client who has sustained a blunt injury to the chest wall. Which finding would indicate the presence of a pneumothorax in this client?
1. A low respiratory rate
2. Diminished breath sounds
3. The presence of a barrel chest
4. A sucking sound at the site of injury
- Diminished breath sounds
Rationale:
This client has sustained a blunt or closed-chest injury. Basic symptoms of a closed pneumothorax are shortness of breath and chest pain. A larger pneumothorax may cause tachypnea, cyanosis, diminished breath sounds, and subcutaneous emphysema. Hyperresonance also may occur on the affected side. A sucking sound at the site of injury would be noted with an open chest injury.
The nurse instructs a client to use the pursed-lip method of breathing and the client asks the nurse about the purpose of this type of breathing. The nurse responds, knowing that the primary purpose of pursed-lip breathing is to promote which outcome?
1. Promote oxygen intake
2. Strengthen the diaphragm
3. Strengthen the intercostal muscles
4. Promote carbon dioxide elimination
- Promote carbon dioxide elimination
Rationale:
Pursed-lip breathing facilitates maximal expiration for clients with obstructive lung disease. This type of breathing allows better expiration by increasing airway pressure that keeps air passages open during exhalation. Options 1, 2, and 3 are not the purposes of this type of breathing.
The nurse is assessing a client with multiple trauma who is at risk for developing acute respiratory distress syndrome. The nurse should assess for which early sign of acute respiratory distress syndrome?
1. Bilateral wheezing
2. Inspiratory crackles
3. Intercostal retractions
4. Increased respiratory rate
- Increased respiratory rate
Rationale:
The earliest detectable sign of acute respiratory distress syndrome is an increased respiratory rate, which can begin from 1 to 96 hours after the initial insult to the body. This is followed by increasing dyspnea, air hunger, retraction of accessory muscles, and cyanosis. Breath sounds may be clear or consist of fine inspiratory crackles or diffuse coarse crackles.
A client has experienced pulmonary embolism. The nurse should assess for which symptom?
1. Hot, flushed feeling
2. Sudden chills and fever
3. Chest pain that occurs suddenly
4. Dyspnea when deep breaths are taken
- Chest pain that occurs suddenly
Rationale:
The most common initial symptom in pulmonary embolism is chest pain that is sudden in onset. The next most commonly reported symptom is dyspnea, which is accompanied by an increased respiratory rate. Other typical symptoms of pulmonary embolism include apprehension and restlessness, tachycardia, cough, and cyanosis.
