W4 Chest Discomfort (Review By Sunday) Flashcards
Chest discomfort causes
Pulmonary:
Pleuritis/Pleurisy
Pneumothorax
Pneumonia
Pleural Effusion
Malignancy
Cardiovascular: MI, angina, pericarditis, aortic dissection, aortic stenosis
GI: GERD, biliary disease, PUD, pancreatitis, esophageal spasm, esophageal perforation
MSK: Costochondritis
Neuro: Herpes neuralgia, spinal radiculopathy
Psychiatry: anxiety, somatoform disorder
Pleurisy/Pleuritis
What is it?
Causes
—Occurs when the pleurae (visceral and/or parietal) become inflamed
—Usually unilateral
—A small amount of pleural fluid is normally present to allow a frictionless environment.
—When inflamed, the membranes rub against one another producing inspiratory, sharp pain and shortness of breath.
Causes:
—Viral Infections (most common): influenza, adenovirus, cytomegalovirus, Epstein-Barr virus, parainfluenza, and RSV
Bacterial Infections
Pulmonary Conditions:
—pneumothorax, asbestosis, mesothelioma, pulmonary embolism , lung cancer
Inflammatory Conditions:
—RA, SLE
Medication Side Effects:
—chemotherapy, amiodarone, hydralazine
Cardiac Conditions:
—heart surgery, pericarditis
Pleurisy/pleuritis
S/S
DX
Signs/Symptoms:
—Pleuritic chest pain: worse with inspiration/expiration, cough, sneezing, or laughing
—Pleural friction rub
—Diminished breath sounds if associated with a pleural effusion (buildup of fluid prevents the pleura from rubbing against one another)
—Dry cough
—SOB
—Fever, chills, and fatigue
Diagnostics:
—Made on history and physical exam with studies attempting to identify the underlying cause
—CBC
—Cultures
—Inflammatory markers
—Chest X-Ray/CT scan
—EKG
—Thoracentesis
Pleurisy/pleuritis
Treatment
Goal is to manage the pain and resolve the underlying cause
—NSAIDS
—PRN antitussive
—Thoracentesis and/or chest tube might be required if to drain an effusion
—Treat underlying cause, i.e., antibiotics for bacterial pneumonia
Costochondritis
What is it
S/S
Management
—Self limiting condition associated with pain to the costochondral junctions of the ribs or chondrosternal joints of the anterior chest wall.
—Clinical diagnosis based on history and physical; does not require specific testing
—Must consider/rule out more severe conditions of chest pain before establishing the diagnosis
History with signs/symptoms:
—Pain is described as worse with movement or a deep breath
—Typically described as DULL or SHARP
—Pain is typically REPRODUCIBLE with palpation with point tenderness where the rib meets the sternum (can affect up to 2 - 5 ribs on average)
—Often occurs with a recent illness associated with a cough or intense exercise
Management
Reassurance
Topical or oral analgesics
Local steroid injections into the joint might assist with inflammation
Acute Respiratory Distress Syndrome (ARDS)
⭐️know for the final
What is it? Know the definition
Hallmarks — 4
What is the patho?
An acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability and a loss of aerated tissue.
HALLMARKS:
—⭐️ Hypoxemia
—⭐️ Bilateral Radiographic Opacities
—⭐️ Diffuse Alveolar Damage
—⭐️ Noncardiogenic Pulmonary Edema
Has a 30-40% mortality that results mostly from extra pulmonary complications — this is what were killing people w/ COVID
PATHOPHYSIOLOGY:
Affected Cells:
—Type I Pneumocytes: thin, flat cells responsible for gas exchange between alveoli and capillaries
—Type II Pneumocytes: smaller cuboidal shaped cells responsible for the secretion of pulmonary surfactant which reduces surface tension in the alveoli and help maintain to keep it open
—An INSULT, either direct (straight into alveoli) or indirect (usually sepsis, systemic), causes release of inflammatory mediators (IL-1, IL-6, TNF) causing neutrophil accumulation in the pulmonary artery circulation
—Neutrophils DAMAGE the vascular and alveolar ENDOTHELIUM (damages the type I and II pneumocytes, damage to surfactant. Preventing gas exchange)
—Leads to PULMONARY EDEMA and impaired gas exchange
—Additionally fibrin debris, WBCs, and RBCs can fill alveoli causing a hyaline membrane and further impaired gas exchange
—Leads to decreased SURFACTANT and loss of surface tension causing collapse of alveoli — further impairs gas exchange
—HYPOXIA — tachypnea, tachycardia
—Final: RESOLUTION stage with repair of type I and II pneumocytes
OR
—FIBROTIC stage: fibroblasts lay thick connective tissue = stiff lungs = restrictive lung pathology
OR
—Die
ARDS
S/S
Indirect and direct lung injuries
know the most common ones
Signs and Symptoms:
—RAPID onset: within 72 hours of an inciting event associated with a rapid worsening clinical condition
—Tachypnea and Tachycardia
—Accessory muscle use
—Dyspnea +/- cyanosis, blue lips, blue fingers
—Crackles, diffuse
—Cough
INDIRECT LUNG INJURY: all start outside the lung
⭐️Sepsis: most common!! ⭐️
lots of vasodilation and vascular permeability, remember because you use vasopressor as treatment. Interstitial and Alveolar EDEMA. Damages alveoli type I and II pneumocytes
—Shock
—Trauma
—Pancreatitis: enzyme releases, cytokine inflammation, cap permeability, damage to pneumocytes
—Drug Overdose: crack, opioids, ASA toxicity
—Blood Transfusion (TRALI) transfusion related acute lung injury, FFP, might have some immune cells from the donor and these can mix and stim an immune process
DIRECT LUNG INJURY:
Occurs to type I and II pneumocytes
⭐️Pneumonia — most common!! ⭐️
—Aspiration
—Pulmonary Embolism
—Near drowning: salt H2O pulls water in from pulmonary capillaries, fresh H2O affects surfactant
—Lung Contusion
—Inhalation Injury
—Oxygen Toxicity
⭐️ARDS ⭐️
Diagnostic criteria
What do you see on CXR?
Management
KNOW THIS
What is the O2 goal?
Diagnostic Criteria (BERLIN DEFINITION):
(A)cute
—onset of symptoms with a known clinical insult of < 1 week
(B)ilateral
—opacities consistent with pulmonary edema based on a chest x-ray or CT scan.
—WHITE FLUFFY CLOUDS: “whited out”
—NO Pleural effusion, lung collapse, and pulmonary nodules
(C)ardiac
—NO cardiac failure and fluid overload
—echo w/o LV failure
—BNP normal
—RHC w PCWP <18 mmHg
(D)ecreased oxygenation must be present
—low P/F ratio
—Pt is HYPOXIC
MANAGEMENT:
—Treat UNDERLYING CAUSE
1. Oxygen Therapy: goal is a PaO2 > 60 mmHg or SpO2 > 90%
2. NIPPV for benefit of PEEP (non-invasive positive pressure ventilation, CPAP, biPAP)
3. If unstable, mechanical ventilation using PEEP and low tidal volumes to prevent ventilator associated injury (tolerate permissive hypercapnia)
—PEEP = keeps alveoli open at the end of expiration, b/c if it closes, due to loss of surfactant, hard to open again
—Aim to minimize or eliminate a positive fluid balance that can worsen pulmonary edema. Might require the use of diuretics
—PRONING to allow better aeration of posterior lung fields
—INHALED Vasodilators: Nitric Oxide or Prostaglandins. Get into capillary to cause vasodilation and improved blood flow to unaffected alveoli for gas exchange
—ECMO (extracorporeal membrane oxygenation)
—Externally pumps and oxygenates a patient’s blood
Acute Respiratory Failure
Two types
Confirm with?
What is the treatment?
TWO TYPES (confirm with ABG):
TYPE I RESPIRATORY FAILURE (HYPOXIA):
—Primarily from failure of OXYGENATION (PaO2 < 60 mmHg, SpO2 <90%)
—Normal or low CO2
—Responds to oxygen therapy
TYPE II RESPIRATORY FAILURE (HYPERCAPNIA):
—Increased CO2 (PaCO2 > 45-50 mmHg)
—Normal or low PaO2
—pH < 7.35
—Failure of VENTILATION (breathing)
—Oxygenation will be affected too
—Requires ventilator support as well as supplemental oxygen (BiPAP, CPAP, to help blow off the CO2)
Acute Respiratory Failure
HYPOXIC RESPIRATORY FAILURE (I):
How is it identified?
Confirmed with?
What can be induced from hypoxia?
—Most patients are initially identified by the presence of a low SaO2 on pulse oximetry
—Followed/confirmed by an ABG.
—Clinically they may appear cyanotic, with tachycardia/tachypnea, accessory muscle use, diaphoresis, anxious/agitated, and/or an altered mental status.
—Cessation of blood flow to the cerebral cortex causes LOC in 10-20 seconds with irreversible changes within 3-5 minutes.
—If tissue PO2 drops, aerobic oxidation converts to anaerobic glycolysis with lactic acidosis (metabolic acidosis)
—Arrhythmias can be induced from hypoxia
Acute Respiratory Failure
HYPERCAPNIC RESPIRATORY FAILURE (Type II):
Increase in?
Causes which symptoms?
How do patients present?
The CO2 retention causes respiratory acidosis (can be exacerbated by tissue hypoxia and metabolic acidosis)
Raised levels of PCO2 increase cerebral blood flow causing a headache, raised CSF pressure, and possibly papilledema.
Patients presents as restless, agitated, with slurred speech, asterixis (flapping tremor), and eventually LETHARGY/SEDATION.
if your patient is altered in the ER or the hospital, don’t just think infection, or sepsis, get an ABG and check CO2 levels
CAUSES of Acute respiratory failure
Type I
DECREASED Fi02 DELIVERY
—High altitude
⭐️HYPOVENTILATION (Minute Ventilation: Respiratory Rate x Tidal Volume)
1. WON’T BREATHE (decreased respiratory rate)
—Sedatives: opiates or benzodiazepines
—CNS pathology: stroke
2. CAN’T BREATHE (decreased tidal volume):
—Chest Wall Deformities: kyphosis, scoliosis, OBESITY, effusion
—Nerve Issue: G. B., Myasthenia Gravis, botulism ALS
—Muscle Pathology: myositis, muscular dystrophy
3. CAN’T BREATHE ENOUGH (small tidal volumes)
—Upper Airway Obstruction: foreign body, MUCUS PLUG, laryngospasm
—Lower Airway Obstruction: COPD, asthma
DIFFUSION IMPAIRMENT (Rare):
—Restrictive interstitial lung disease
—ARDS, pulmonary edema
SHUNT (Worst): mixing of deoxygenated with oxygenated blood
—Cardiac with blood movement from R -> L: ASD, VSD, PDA
—Pulmonary AVM where pulmonary vein and artery connect and bypass/eliminate capillaries which are needed for gas exchange
VENTILATION-PERFUSION (V/Q) MISMATCH (Most Common):
—Blood moving through pulmonary capillaries without picking up ENOUGH oxygen from alveoli
—Results from impaired alveolar airspace filling from obstruction, pus, water, or blood (ventilation) OR a pulmonary embolism (perfusion)
1. AIRWAY: mucus plug, COPD, asthma
2. ALVEOLI: atelectasis/collapse, PNA-pus, ARDS-edema, Cardiogenic-edema, Alveolar Hemorrhage-blood
3. PULMONARY VESSELS: pulmonary embolism
Type (II) Respiratory Failure - Causes
HYPOVENTILATION (it’s always this!)
—Alveolar ventilation is insufficient to excrete CO2 produced from tissue metabolism
—DECREASED MINUTE VENTILATION (equals respiratory rate x tidal volume)
—INCREASED CO2 PRODUCTION leads to ACIDOSIS
(CO2) + (H20) –-> H2CO3 —-> (H+) + (HCO3-)
DIAGNOSED with pH < 7.35 and PaCO2 > 45-50 mmHg
WON’T BREATHE — decreased respiratory rate (CNS and sedatives)
CAN’T BREATHE — decreased tidal volume (chest wall, neuromuscular)
CAN’T BREATHE ENOUGH — decreased tidal volume (obstructive lung disease - COPD/asthma, mucus plug)
Respiratory Failure - Diagnosis
Identified by ⭐️low SpO2 < 90% ⭐️ (worse if on oxygen and remains low)
STEP I: acquire an ABG
—If have a low PaO2 then have hypoxic respiratory failure (type I) = oxygen therapy
—If only have high an elevated PaCO2 or additionally have an elevated PaCO2 with the low PaO2, then have hypercarbic (type II) respiratory failure
STEP II:
—if with hypoxemia, acquire the A-a O2 gradient which indicates a problem with gas exchange
—If elevated, then problem is related to DIFFUSION, V-Q MISMATCH, or SHUNT
—If normal, then related to HYPOVENTILATION or DECREASED FiO2
**TIP: If have an elevated PaCO2, cause if HYPOVENTILATION and do not necessarily need to acquire an A-a O2 gradient
**TIP: Hypoxia that does not respond to supplemental 100% FiO2, likely a shunt. If responds, likely V-Q mismatch (most common).
**TIP: In the rare case you have a low PaO2 with NORMAL A-a O2 gradient (no V/Q mismatch) and NORMAL PaCO2 (so not hypoventilating), the cause is low FiO2 delivery usually from high altitude states
Other testing:
Chest X-ray and/or CT chest for imaging of underlying cause
Bronchoscopy (mucus plug)
Respiratory Failure - Treatment
Type I
What is the goal for oxygenation FiO2?
if still hypoxic with O2, then what?
Type II
Type (I) Treatment
TREAT UNDERLYING CAUSE:
—Bronchodilators for COPD
—Antibiotics if PNA
—Diuretics for edema
—Suction secretions for mucus plug
—Reversal agents for sedation
—Thoracentesis for effusion
—MONITOR with serial ABGS
OXYGENATION (non-invasive): nasal cannula, face mask, venturi mask
—Goal is ~60% max FiO2 (if greater, at risk of O2 toxicity if extends >24 hours)
—If remain hypoxic despite 60% FiO2, then add PEEP (positive end expiratory pressure) or pressure that will remain in the lungs at the end of exhalation with goal to keep alveoli open for gas exchange. PEEP decreases derecruitment.
NON-INVASIVE MECHANICAL VENTILATION (PEEP):
—CPAP (continuous positive airway pressure, this can be uncomfortable because its pushing air in when you’re exhaling)
—BiPAP (bilevel positive airway pressure; IPAP and EPAP, inspiratory and expiratory, more support when the inhale and drop it down on exhale so it’s easier to exhale. Need 5cm to keep the PEEP open, EPAP)
INVASIVE MECHANICAL VENTILATION:
—ET tube or tracheostomy
Type (II) Respiratory Failure - Treatment
—TREAT UNDERLYING CAUSE (ex: Narcan for opioid overdose)
—IMPROVE MINUTE VENTILATION (INCREASE RESPIRATORY RATE OR INCREASE TIDAL VOLUME)
—NON-INVASIVE MECHANICAL VENTILATION (CPAP, BiPAP, this is basically the treatment for hypercapnia, blow off the CO2)
—INVASIVE MECHANICAL VENTILATION (Intubation)
OXYGENATION
—Achieve safe oxygen concentration without increasing CO2 and acidosis
MONITOR Serial ABGs
[SKILLS OSCE]
What is this?
ARDS
Non-invasive positive pressure ventilation
Mechanical reference
