Show Menu
Cheatography
  1. Home >
  2. Cheat Sheets >

ACNP Pulmonary Respiratory Failure Cheat Sheet (DRAFT) by

ACNP Student Pulmonary Rotation

This is a draft cheat sheet. It is a work in progress and is not finished yet.

Hypoxemia

Workup
Get PaCO2 level, A-a gradient, and response to supple­mental O2.
If PaCO2 is elevated
• Hypove­nti­lation is occurring.
• If the A-a gradient is normal, hypove­nti­lation or low inspired PO2 is the only mechanism.
• If the A-a gradient is increased, hypove­nti­lation is not the lone mechanism of hypoxemia.
If PaCO2 is not elevated
• No hypove­nti­lation.
• If A-a gradient is not increased, low inspired PaO2 is the cause of hypoxemia.
If A-a gradient is increased
• With low to normal PaCO2. See if the lowered PaO2 is improved with supple­mental O2. If so, there is V/Q mismatch. If it does not improve, shunting is present.
V/Q Mismatch
• Typically leads to hypoxia without hyperc­apnia (PaCO2 is usually low to normal).
• Most common mechanism of hypoxemia (esp. in chronic lung disease).
• Responsive to supple­mental oxygen.
• Ventil­ation without perfusion.
Intrap­ulm­onary Shunting
• Little or no ventil­ation in perfused areas due to collapsed or fluid-­filled alveoli.
• Venous blood is shunted into the arterial circul­ation without being oxygen­ated.
• Perfusion without ventil­ation.
•Causes include atelec­tasis or fluid buildup in alveoli (pneumonia or edema) or direct right to left intrac­ardiac blood flow in congenital heart disease.
• No responsive to supple­mental oxygen.
Hypove­nti­lation
Leads to hyperc­apnia with secondary hypoxemia.
Increased CO2 production
In sepsis, DKA, hypert­hermia, etc. Leads to hyperc­apnic respir­atory failure.
Diffusion Impairment
In ILD causes hypoxemia without hyperc­apnia.

Hypoxemic Failure

Hypoxia
PaO2<6­0mmHg and PaCO2>­50mmHg.
• Severe hypoxemia can result in irreve­rsible damage to CNS and CVS, and must be corrected rapidly.
• O2 saturation is <90% despite FiO2>0.6.
• Causes include lung pathology like ARDS, severe pneumonia, and pulmonary edema.
• V/Q mismatch and intrap­ulm­onary shunting are the major pathop­hys­iologic mechan­isms.

Oxygen Delivery

Low Flow
• Nasal cannula has flow rate of 1-6L/min, FiO2 up to 0.40, is easy to use and comfor­table.
• Simple face masks have a flow rate of 1-10L/min, FiO2 of 0.40-0.60, and can deliver higher flow rates than nasal cannula.
High Flow
• Venturi masks have a flow rate of 4-10L/min, FiO2 up to 0.50 with precise measur­ements, and are preferred in CO2 retainers due to higher precision and control of oxygen­ation.
• Nonreb­reather masks have flow rates up to 15L/min, FiO2 up to 0.70-0.80, and can achieve higher FiO2 at lower flow rates.
NPPV
• BIPAP or CPAP via nasal mask or full-face mask. Indicated in patients in impending respir­atory failure to avoid intubation or mechanical ventil­ation.
• Success is highest in hyperc­arbic respir­atory failure (esp. COPD). Patient must be neurol­ogi­cally intact, awake, cooper­ative, and able to protect their airway.
 

Acute Respir­atory Failure

Pathop­hys­iology
Results when there is inadequate oxygenate of blood or inadequate ventil­ation or both.
Symptoms
dyspnea is the first. Cough may or may not be present, depending on the underlying cause.
Signs
Inability to speak in complete sentences, use of accessory muscles tachypnea, tachyc­ardia, cyanosis, impaired mentation (due to fatigue or hyperc­apnia, of if cause of respir­atory failure is CNS depres­sion).
Causes
• CNS Causes: depression or insult from drug overdose, stroke, or trauma.
• Neurom­uscular Causes: myasthenia gravis, polio, Guilla­in-­Barre syndrome, amyotr­ophic lateral sclerosis.
• Upper Airway Causes: obstru­ction due to stenoses, spasms, or paralysis.
• Thorax and Pleural Causes: mechanical restri­ction due to kyphos­col­iosis, flail chest or hemoth­roax.
• CVS and Heme Causes: CHF, valvular diseases, PE, and anemia.
• Lower Airway Causes: asthma, COPD, pneumonia, ARDS.
Diagnosis
ABG, CXR, CT, CBC, BMP, and consider cardiac enzymes if pulmonary edema is suspected.

Hyperc­arbic Failure

Hyperc­apnia
• PCO2>5­0mmHg.
• Severe hyperc­apnia can lead to dyspnea and vasodi­lation of cerebral vessels (with increased ICP and subsequent papill­edema, HA, impaired consci­ous­ness, and finally coma).
• A failure of alveolar ventil­ation.
• Either a decrease in minute ventil­ation or an increase in physio­logic dead space that leads to CO2 retention and eventually hypoxemia.
• May be caused by underlying lung disease (COPD, asthma, CF, severe bronch­itis) or without lung disease (patients with impaired ventil­ation due to neurom­uscular diseases, CNS depres­sion, mechanical restri­ction of the chest, or respir­atory fatigue). Also increased CO2 production or diffusion impair­ment.
• Hyperc­apnia can be caused by hypove­nti­lation (secondary to a variety of causes).
•Respir­atory acidosis occurs when hyperc­apnia is present.
• If chronic acidosis, renal compen­sation occurs and acidosis is less severe.

Treatment


• Treat underlying disorder with bronch­odi­lators, cortic­ost­eroids, antibi­otics, etc.
• Provide supple­mental oxygen if hypoxemic. In hypoxemic failure, use lowest concen­tration of oxygen that provides sufficient oxygen­ation to avoid oxygen toxicity (due to free radicals).
• In hyperc­arbic failure, tradit­ionally do not give high concen­tra­tions of O2, especially in patients with COPD to not depress respir­atory drive. Apply NPPV only for conscious patients. Intubation and mechanical ventil­ation
 

Acute Respir­atory Distress Syndrome

Pathop­hys­iology
• A diffuse inflam­matory process involving both lungs. Neutro­phils are activated in the systemic or pulmonary circul­ations.
• Not a primary disease but a disorder that arises from other conditions that cause a widespread inflam­matory process.
• There is massive intrap­ulm­onary shunting, decreased pulmonary compliance (increased work), increased dead space (secondary to obstru­ction and destru­ction of pulmonary capillary bed), low VC, and low FRC.
Intrap­ulm­onary Shunting
• Severe hypoxemia with no signif­icant improv­ement on 100% oxygen.
• Shunting secondary to widespread atelec­tasis, collapse of alveoli, and surfactant dysfun­ction.
• Inters­titial edema and alveolar collapse are due to increased lung fluid that leads to stiff lungs, an increase in A-a gradient, and ineffe­ctive gas exchange.
• Effects of the increase in pulmonary fluid are identical to those in cardio­genic pulmonary edema, but the cause is increased alveolar capillary permea­bility
Causes
• Sepsis is the most common (which can itself be secondary to pneumonia, urosepsis, wound infect­ions, etc). Aspiration of gastric contents, severe trauma, fractures (femur, pelvis), acute pancre­atitis, multiple or massive transf­usions, near-d­row­ning, drug overdose, toxic inhala­tion, intrac­ranial HTN, and cardio­pul­monary bypass.
Signs
• Dyspnea, tachypnea, tachyc­ardia due to increased work of breathing.
• Progre­ssive hypoxemia not responsive to supple­mental oxygen (ratio of PaO2 to FiO2<200).
• Patients are difficult to ventilate because of high peak airway pressures due to stiff, noncom­pliant lungs.
Diagnosis
• Hypoxemia that is refractory to oxygen therapy (ratio of PaO2/F­iO2­<20­0-300), bilateral diffuse pulmonary infilt­rates on CXR, no evidence of CHF (PCWP <18­mmHg).
CXR
• Shows diffuse bilateral pulmonary infilt­rates. Improv­ement on CXR follows clinical improv­ement after 1-2 weeks.
Arterial Blood Gas
• Hypoxemia (PaO2<­60mmHg).
• Initially, respir­atory alkalosis (PaCo2­<40) is present, which gives way to respir­atory acidosis as the work of breathing increases and PaCO2 increases.
• If patient is septic, metabolic acidosis may be present with or without respir­atory compen­sation.
Pulmonary Artery Catheter
• Enables a determ­ination of PCWP, which reflects left heart filling pressures and is an indirect marker of intrav­ascular volume status.
• The most useful parameter in differ­ent­iating ARDS from cardio­genic pulmonary edema.
• If PCWP is <18­mmHg, ARDS is more likely, whereas if PCWP is >18­mmHg, cardio­genic is more likely.
Bronch­oscopy
With bronch­oal­veolar lavage. May be considered if patient is acutely ill and infection is consid­ered. Fluid collected can be cultured and analyzed for cell differ­ential, cytology, Gram stain, and silver stain.
Treatment
• Oxygen­ation >90%. Mechanical ventil­ation with PEEP is usually required (increases lung volume by opening collapsed alveoli and decreasing shunting).
• Avoid volume overload and maintain low-normal intrav­ascular volume (PCWP 12-15m­mHg).
• Vasopr­essors may be needed to maintain BP.
• Patients with sepsis have high fluid requir­ements, so this might be difficult. Treat underlying cause. Tube feedings are preferred over parenteral nutrition.
.