Respiratory Failure

Hypercapnic resp. failure: PaCO2 >45 - 55 mm Hg (50 mmHg), pH < 7.3 @RA producing respiratory acidosis.

Usually involves some combinations of the following three processes:

• Increased CO2 production - respiratory acidosis: can occur in fever, sepsis, seizures, and excessive -CHO loads in patients with underlying lung disease. Oxidation of -CHO fuels is associated with more CO2 production per molecule of O2 consumed as compared to the oxidation of fat fuels.

• Increased dead space occurs when large areas of the lungs are ventilated but not perfused or when the region of the lung is perfused more than it is ventilated. Seen in intrinsic lung diseases like COPD, asthma, CF, pulmonary fibrosis. Chest wall d/o with parenchymal abnormalities like scoliosis. Usually, these d/o are associated with widened P(A-a)O2 gradients.

• Decreased minute ventilation can result from spinal cord lesions, GBS, botulism, myasthenia gravis, ALS, PM, muscular dystrophy, thoracoplasty, scoliosis, drug OD, myxedema, hypokalemia, and upper airway obstruction. These d/o are usually associated with a normal P(A-a)O2 gradient unless accompanying lung disease is also present.

• CO2 retainers: COPD, asthma, OSA, obesity hypoventilation syndrome, chest wall trauma, neuromuscular dz (GB synd.), CNS depression or drug OD.

Hypoxic resp. failure: occurs when normal gas exchange is seriously impaired. PaO2 <60 mm Hg or arterial oxygen saturation SaO2 <90%, pH < 7.3. @RA, tachypnea and hypocapnia. However, its progression can lead to hypercapnia as well.

• ARDS is a form of respiratory failure caused by acute lung injury. Diruption of alveolar-capillary membrane, leading to increased vascular permeability and accumulation of inflammatory cells and protein-rich edema fluid within the alveolar space.

  • American-European Consensus Conference has defined ARDS as follows:

    • Acute bilateral infiltrates

    • Ratio of PaO2 to FiO2 <200, and

    • No evidence of heart failure or volume overload as the principal cause of the pulmonary infiltrates

  • FiO2 expressed as a decimal (e.g., room air is 0.21).

  • For example, if pO2 is 100/0.21, the ratio is 476.

  • PAWP 18 mm Hg or less or no clinical evidence of eleveated left atrial pressure on the basis of CXR or other clinical data.

• Hypoxic respiratory failure occurs due to one of the following six processes:

  • Shunt

    • It is the fraction of mixed venous blood that passes into the systemic arterial circulation after bypassing the functioning lung units. Congenital shunts are due to developmental anomalies of the heart and great vessels. Acquired shunts usually result from diseases that affect lung units, although cardiac and peripheral vascular shunts also can occur. Shunts are associated with a widened P(A-a)O2 gradient, and the resultant hypoxemia is resistant to correction with supplemental O2 alone when the shunt fraction of the CO is >30% (>30% of CO is getting shunted).

  • V/Q mismatch

    • COPD, asthma, pneumonia, sarcoidosis, PE often produce lung regions with abnormal V/Q. Usually, by increasing FiO2 there is an increase in PaO2.

  • Low FiO2

    • Usually, FiO2 is reduced at high altitudes or when toxic gases are inhaled.

  • Hypoventilation

    • Associated with elevated PaCO2 values, and the resultant hypoxemia is due to increased alveolar CO2, which displaces O2. Usually, O2 therapy improves hypoxemia as a result of hypoventilation but may worsen the overall degree of hypoventilation, especially in Pts with COPD. Primary treatment is directed at correcting the cause of the hypoventilation.

  • Diffusion impairment

    • Hypoxemia due to diffusion impairments usually responds to supplemental O2 therapy, as is seen in Pts with ILD.

  • Low mixed venous oxygenation

    • Normally, the lungs fully oxygenate pulmonary arterial blood, and mixed venous oxygen tension (PvO2) does not affect PaO2 significantly. However, a decreased PvO2 can lower the PaO2 significantly when either intrapulmonary shunting or V/Q mismatch is present. Factors that can contribute to low mixed venous oxygenation include anemia, hypoxemia, inadequate CO, and increased O2 consumption. Improving O2 delivery to tissues by increasing Hb or CO usually decreases O2 extraction and improves SvO2.

  • Mixed respiratory failure

    • Seen most commonly after surgery, especially in patients with underlying lung disease who are undergoing upper abdominal procedures. Atelectasis often multifactorial - decreased lung volumes and cough due to the effects of anesthesia; abnormal diaphragmatic function from surgery or associated pain, and interstitial edema causing small airways to close. Phrenic nerve injury can also cause it.

Causes of shunts and hypoxic respiratory failure

• • Cardiogenic pulmonary edema (low permeability, high hydrostatic pressure): AMI, LVF, MR, MS, Diastolic dysfunction.

  • Noncardiogenic pulmonary edema (high permeability, low hydrostatic pressure): Sepsis, aspiration, multiple trauma, pancreatitis, near-drowning, pneumonia, reperfusion injury, inhalation injury, drug reaction (ASA, narcotics, interleukin-2).

  • Mixed pulmonary edema (high permeability, high hydrostatic pressure): AMI, volume overload associated with sepsis, aspiration, high altitude exposure.

  • Pulmonary edema of unclear etiology: upper airway obstruction, neurogenic cause, lung rexpansion.

  • Hepatopulmonary syndrome: Desaturation on pulse oximetry with change in body position with increase in A - a gradient. Tx: Liver transplant, O2.

ALI: PaO2/FiO2 <300.

• Vent settings: Low tidal vol. max FiO2, high PEEP ~9. Plateau pressure <30 cm H2O.

• Increase PEEP first, then FiO2.

A-a O2 gradient

• Differentiates intrinsic pulmonary from extrapulmonary disease.

• A-a O2 gradient = PAO2 - PaO2

• PAO2 = (atmospheric pressure - water vapor pressure) FiO2 - (PaCO2/0.8)

• PAO2 =( FiO2 x 713) - (PaCO2/0.8)

• For Pts at sea level breathing room air, PAO2 can be determined by

  • PAO2 = 150 - (PaCO2/0.8).

• PaO2 is measure by ABG.

• A - a = (150 - [1.25 x PaCO2] - PaO2). Use this formula.

• Normal A-a gradient is 5 - 20 mmHg.

• An A-a gradient > 20 implies intrinsic pulmonary disease causing impaired gas exchange.

Impending neuromuscular failure: “20/30/40” rule:

• • Tachypnea, tachycardia, paradoxical breathing

  • Vital capacity: <20 mL/kg (normal adult, 40-70 mL/kg)

  • Maximum inspiratory pressure: –30 cm H2O (normal, –70 to –100 cm H2O)

  • Maximum expiratory pressure: 40 cm H2O (normal, 140-200 cm H2O)

Treatment strategies:

• Evaluate the patient immediately

• ABC. Head/jaw postitioning/OP, NP airways/LMA

• Oxygen

  • nasal cannula up to 4 L

  • 40% Venturi Mask

  • 100% nonrebreather mask

• Hold narcotic analgesics

• If pupillary constriction - opiate toxicity, give naloxone hcl 0.2 - 2 mg IV STAT

• Keep SpO2 >92%

• NIPSV by facemask

• Albuterol/Atrovent breathing treatment if wheezes present

• STAT Portable Chest X-ray

• Consider getting an Arterial Blood Gas

• pH <7.20 requires intubation.

• Endotracheal intubation indications:

  • Initiation of mechanical ventilation

  • Airway protection

  • Inadequate oxygenation using less invasive methods

  • Prevention of aspiration and allowing for suctioning of pulmonary secretions

  • Hyperventilation for the treatment of increased ICP.

KEY CONCEPTS

• • Tracheal cuff pressures <25 mm Hg (below capillary filling pressure) to prevent ischemic mucosal injury.

  • Improper ETT positioning is the most important and immediate complication that must be recognized and corrected promptly.

    • Tip of ETT should be 3 - 5 cm above carina.

• Pt with hypoxemia on ABG: increase FiO2 and/or PEEP.

• Pt with hypercapnea (raised PaCO2 and low pH)/ventilating poorly: increase minute ventilation = increase tidal volume and/or rate.

Intubation:

Indications:

Failure to protect airway, oxygenation, ventilation, neurological worsening, expanding neck mass, planned surgery, status epilepticus management.

Pt. SpO2: <90% or PaO2 <60 mm Hg, is retaining CO2, signs of resp. distress (dyspnea, retracting, nasal flaring, paradoxical abdominal breathing, cyanosis), or is not protecting the airway due to neurologic injury:

• • BVM w/ 100% O2 @ rate: 12 bpm.

  • Brief hyperventilation can reduce ICP in patients who are herniating, but prolonged hyperventilation to a PaCO2 <25 mm Hg is not recommended, as this can precipitate cerebral ischemia.

  • Pts with craniofacial trauma are at risk for pneumocephalus with BVM. This risk should be assessed prior to bagging such patients, and preemptive controlled intubation should be undertaken when necessary.

  • Difficult airway, call an experienced anesthesiologist.

  • If extremely difficult airway, call otolaryngologist to do bedside trach.

  • IVF, CVC

  • Medications at the bedside, besides intubation cart: propofol, etomidate, NMBA, phenylephrine, and/or ephedrine.

  • LMA of the appropriate size should be readily available for the patient in whom intubation is anticipated to be difficult.

History:

• • Mechanism of injury (cranifacial, cervical, thoracic, pulmonary or SCI)

  • H/o difficult airway, prolonged intubation, head or neck radiation or surgery, RA (atlantoaxial subluxation), Down's syndrome (abnormal airway anatomy and atlantoaxial subluxation), ankylosing spondylitis, tracheostomy.

  • Cardiac, pulmonary, smoking, last ingestion (aspiration risk).

(H LEMOON)

PE:

• • MS, CN, motor, cerebellar, sensory, reflexes

  • Look externally:

    • Abnormal facial shape, facial hair, overhanging incisors, narrow mouth, inability to protrude mandible, micrognathia, poor TMJ mobility, long, high-arched palate, short, thick neck; tracheal deviation, presence of vomitus or blood in oropharynx.

  • Evaluate the 3-3-2 rule:

    • Mouth opening <3 finger breadths (4 cm)

    • Hyaloid-chin distance <3 finger breadths (4 cm)

    • Thyroid cartilage-floor of mouth <2 finger breadths.

  • Mallampati classification (best performed when Pt. is sitting, tongue protruding, and not phonating):

    • Class I: fully visible tonsils, uvula, and soft palate

    • Class II: visibility of hard and soft palate and upper portion of the tonsils and uvula

    • Class III: Soft and hard palate and base of uvular are visible

    • Class IV: Only hard palate visible

  • Obstruction/Obesity: Airway obstruction, pathology, tumor, secretions, muffled (hot-potato voice). BMI >30 kg/m2 and/or neck circumference >60 cm.

  • Neck mobility: limited ROM, halo or neck immobilization devices. History of cervical instrumentation.

  • Elevated ICP

  • Cranifacial trauma

  • C-spine immobilization

American Society of Anesthesiology has suggested a period of 2 hours after the ingestion of clear liquids, 6 hours after a "light meal," and 8 hours after a meal of fried or fatty food to be used as a guideline for surgical patients undergoing elective surgical procedures.

Avoid ▲ ICP while intubating: Minimize laryngeal stimulation. Lidocaine, 1%, 1 ml/kg IV suppresses the cough reflex, may lower cerebral O2 demand, reduces bronchospasm, and should be used in patients with suspected elevated ICP.

Intubation:

• • Equipment and Preparation: Mac #3, or #4, curved blade, Miller #3 or #4. Glidescope

  • Equipment Checklist:

  • ETT with a stylet (8 in men, 7 in women)

  • Ambu bag w/ PEEP device attached to 100% O2.

  • Suction

  • 10 mL syringe

  • Intubating laryngeal mask airway

  • Capnometer/CO2 detector

  • Oral and nasal airway

  • Tape and tincture or benzoin

  • Check the ETT cuff, laryngoscope light, C/I to medications, free-flowing IV access, BP, O2, HR, cardiac monitoring.

  • In case of hypotension: keep phenylephrine, 0.5-5 mcg/kg/min cIV.

  • Position Pt.

  • Pretreatment:

    • Preoxygenate w/ 100% O2 for 1 min, and ensure SpO2: 95%.

    • Induction: Paralysis is not always necessary. Try to avoid in neurologic patients, however, have them available for safe intubation.

      • Induction medications:

        • Propofol: 1.5- 2.5 mg/kg for induction.

          • Dose unchanged by renal or liver disease. No active metabolite.

          • Associated with hypotension and bradycardia (in volume depleted patients)

          • Causes Cardiosuppression, immunosuppression

          • Large lipid load can cause pancreatitis.

          • PRIS: Propofol induced infusion syd: Typically doses >5mg/kg/h and associated with lactic acidosis, rhabdomyolysis, renal failure, hyperkalemia, cardiovascular collapse, and death. Common in children, but has been described in adults as well. Concomittant use of steroids and sympathomimetics can increase the risk of PRIS.

        • Etomidate: 0.2-0.5 mg/kg.

          • Dose unchanged by renal or liver disease.

          • Does not cause hypotension or cardiosuppression.

          • Inhibits adrenal steroidogenesis via inhibition of mitochondrial hydroxylase, even after a single dose.

          • Can cause delayed hypotension due to adrenal insufficiency, particularly in patients previously medicated with steroids.

          • Caution in patients with sepsis.

        • Ketamine: 1-2 mg/kg IV; 5-10 mg/kg IM

          • Dose unchanged by renal or liver disease.

          • Bronchodilator

          • May ▲ ICP, HTN, tachycardia, arrhythmias, dissociative psychological effects, and delerium.

      • Paralytic agents: Prolonged neuromuscular blockade has been described with both aminosteroids and benzylisoquinoliniums. Risk factors for prolonged blockade include organ dysfunction, sepsis, magnesium therapy, acidosis, steroid therapy, and prolonged infusion. Use TOF (train of four) to check for prolonged blockade (anything less than 4 strong twitches suggest blockade). Infusion of NMBA increases the risk of ICU myopathy/neuropathy.

        • Succinylcholine: depolarizing.

          • Induction: 0.6 mg/kg IV or 3-4 mg/kg IM

          • Dose unchanged in renal disease. Has prolonged effect in liver disease.

          • Prolonged paralysis in those with pseudocholinesterase deficiency.

          • Can cause malignant hyperkalemia in Pts immobilized >24 h (due to upregulation of extrajunctional embryonic nicotinic receptors), patients with neurologic injury, crush injuries, burns, or preexisting hyperkalemia. Malignant hyperthermia is related to a defect in ryanodine receptor. Can cause elevated ICP and IOP. Not recommended in most Neuro-ICU patients.

          • Pancuronium

            • 0.1-2 mg/kg IV

          • Cistracurium

            • 0.2 mg/kg

          • Rocuronium: non-depolarizing aminosteroid

            • 0.6 mg/kg IV

    • Sedatives:

      • • Fentanyl

        • Morphine

        • Hydromorphone:

          • can be used in renal failure (whereas fentanyl and morphine accumulate)

        • Propofol

        • Midazolam

        • Lorazepam

        • Dexmedetomidine: Central alpha-2 agonist, analgesic, anti-shivering, hypnotic, and anxiolytic

          • 0.5 mcg/kg IV

          • cIV: 0.2-0.7 mcg/kg/h IV

          • Minimal respiratory or neurologic depression

          • Hypotension and bradycardia with bolus dosing.

          • Can reduce CBF

          • C/I in heart block.

          • No active metabolite.

          • Synergestic with other sedatives/analgesics, particularly opiates.

          • Can cause withdrawal sx similar to clonidine, with long duration.

          • Inhibits cortisol synthesis at high doses.