Rosen & Barkin's 5-Minute Emergency Medicine Consult (762 page)

Basic modes of ventilation:

• Early, classic modes of ventilation allowed for only simple ventilator/patient interaction and limited control of small number of variables
  
• Continuous mandatory ventilation (CMV)
  :
  
  • CMV is the classic mode where only 1 variable can be set
    
  • Allows for NO interaction between the patient and the ventilator—all breaths are fully controlled breaths
    
  • Breaths are delivered only at a set rate—time is the trigger for every breath
    
  • Breaths are defined only by the control:
    
    • Volume controlled (also known as volume cycled) CMV: Delivers set volume with each breath and guarantees certain MV
      
    • Pressure controlled (also known as pressure cycled) CMV: Delivers constant flow of gas until set inspiratory pressure reached which guarantees peak pressures will be reasonable
      
    • The variable that is not set cannot be controlled (i.e., may have very high peak inspiratory pressures in order to deliver a certain TV or may dangerously hypoventilate in order to keep safe airway pressures)
      
• Assist–control (AC)
  :
  
  • Similar to CMV in that all breaths are the same controlled breaths based on machine determined variables
    
  • In AC, patient can trigger a breath, but the same machine controlled breath is delivered
    
  • Spontaneous breath trigger is either the reduction in airway pressure or the increase in air flow as patient initiates breath
    
• Intermittent mandatory ventilation (IMV)
  :
  
  • Delivers controlled breath at set RR
    
  • Patient may breath spontaneously between these breaths; however:
    
    • Spontaneous breaths are not supported
      
    • Can lead to breath stacking as ventilator does not take patient’s spontaneous breaths into consideration
      
  • In some IMV modes, spontaneous breaths can be pressure supported, but this is not the rule
    
• Synchronous intermittent mandatory ventilation (SIMV)
  :
  
  • Same as IMV, but ventilator tries to synchronize patient’s spontaneous breaths with those set by RR
    
  • Lowers risk of breath stacking
    
• Pressure support ventilation (PSV)
  :
  
  • Ventilator augments patient’s spontaneous breaths with set amount of pressure
    
  • If support is adequate to meet needed driving pressure and patient is able to initiate breaths, often most comfortable mode
    
• Most modern ventilators and newer modes allow for much more complex interaction between ventilator and patient as well as increased control of multiple variables:
  
  • Newer modes are quite variable and are dependent on patient specifics.
    
  • May be dynamic combination of more traditional types of breaths as described below
    
  • Can often tailor breath delivery to optimize mechanics in specific disease process
    
• Risks of mechanical ventilation:
  
  • Ventilator-induced lung injury (VILI): Overdistension caused by high pulmonary pressures leads to inflammation and alveolar injury
    
  • Derecruitment injury: Inflammation and injury caused by repetitive opening and collapse of alveoli; can be reduced with appropriate use of PEEP
    
  • Barotrauma outside lungs due to cyclical reinflation (i.e., pneumothorax, pneumoperitoneum, subcutaneous emphysema)
    
  • Oxygen toxicity
    
  • Decreased venous return and subsequent drop in cardiac output/BP due to elevated intrathoracic pressures
    
  • Increased V/Q mismatch due to altered pattern of gas delivery (alveoli that usually do not get significant gas delivery in natural breathing will be responsible for more gas exchange without any augmented blood supply AND overdistension of alveoli may cause compression of alveolar blood supply)
    
  • Loss of upper airway defenses against infection
    
  • Associated risks of sedation (delirium, increased immobility, prolonged illness, etc.)
    
  • Associated risks of immobility (severe myopathy, thrombosis, prolonged illness, etc.)
    
  • Stress ulcer formation
    
  • Problems related to endotracheal tube or tracheostomy such as tracheomalacia or vocal cord paralysis
    

• Sedation and analgesia strategies should prioritize pain control, target the lowest level of sedation possible, and utilize intermittent bolus therapy before resorting to infusion
  
• Oversedation and benzodiazepines are both associated with risk of critical illness delirium
  
• Propofol: 0.3–1 mg/kg IV loading dose, maintenance initiated at 5–50 μg/kg/min IV infusion. Causes vasodilation and associated hypotension. Especially with bolus loading dose. Risk of propofol infusion syndrome with prolonged infusions.
  
• Dexmedetomidine: 0.2–1.4 μg/kg/h. Can be used with loading bolus of 1 μg/kg. Does not cause respiratory depression. Can be associated with significant bradycardia.
  
• Ketamine: Load 1–3 mg/kg with maintenance 1–2
  mg/kg/h. Potential benefit is avoiding hemodynamic instability seen with many other agents. Benzodiazepine dosing prior to emergence can help prevent emergence nightmares. There is controversy about using ketamine in patients with elevated intracranial pressures, but it may actually help maintain cerebral perfusion pressure in mechanically ventilated patients.
  
• Fentanyl: Bolus 0.5–1.5 μg/kg IM or slow IV. Infusion rates start at 1 μg/kg/h. Consider prior opiate exposure when dosing.
  
• Albuterol: 2.5–5 mg/5 mL saline q4h via in-line endotracheal delivery
  
• Ipratropium bromide: 0.5 mg/2.5 saline q4h vial in-line endotracheal delivery
  

FOLLOW-UP

ICU admission required for all intubated patients

• Physiology can help you troubleshoot the vent. Remember that you control ventilation by adjusting the TV and RR and that you control oxygenation by adjusting PEEP and FiO
  ₂
  . Peak pressure is determined by airway resistance. Elevated peak pressures can be caused by problems such as bronchospasm, secretions, or kinked tubes. Plateau pressure is determined by lung and chest wall compliance. Elevated plateau pressures can be caused by problems such as ARDS, pulmonary fibrosis, obesity, or edema.
  
• Knowing the indication for mechanical ventilation is key to choosing the most appropriate and least harmful mode of ventilation and ventilator settings
  
• It is important to understand whether a breath is controlled or assisted, what triggers a breath, and how the breath is given in order to understand modes of ventilation. Most modern modes of ventilation are a complex combination of different types of breaths based upon goals set by the clinician or interactions with the patient.
  
• ARDS requires low TV ventilation and open lung ventilatory strategies can be used for severe cases
  
• Remember to allow time for full expiration for patients with obstructive airway disease
  

• Gabrielli A, Layon AJ, Yu M, eds.
  Critical Care.
  4th ed. Philadelphia, PA: Wolters Kluwer, Lippincott Wiliams and Wilkins; 2009.
  
• Gattinoni L, Protti A, Caironi P, et al. Ventilator-induced lung injury: The anatomical and physiological framework.
  Crit Care Med
  . 2010;30:S539–S548.
  
• Nagler J, Krauss B. Capnography: A valuable tool for airway management.
  Emerg Med Clin North Am.
  2008;26:881–897.
  
• Serpa Neto A, Cardoso SO, Manetta JA, et al. Association between use of lung-protective ventilation with lower tidal volumes and clinical outcomes in patients without acute respiratory distress syndrome: A meta-analysis.
  JAMA.
  2012;16:1651–1659.
  
• Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Network.
  N Engl J Med.
  2000;18:1301–1308.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Dyspnea
  
• Respiratory Distress
  

CODES

V46.11 Dependence on respirator, status

BASICS

• Ventricular fibrillation (VF) is completely disorganized depolarization and contraction of small areas of the ventricle without effective cardiac output.
  
• Cardiac monitor displays absence of QRS complexes and T-waves with the presence of high-frequency, irregular undulations that are variable in both amplitude and periodicity.
  

• Damaged myocardium creates sites for re-entrant circuits:
  
  • Myocardial damage may be caused by multiple factors including ischemia, necrosis, reperfusion, healing, and scar formation
    
• Most often a result of severe myocardial ischemia:
  
  • 7% of patients with STEMI develop sustained VF, 80–85% occurring in the 1st 24 hr
    
• Complication of cardiomyopathy:
  
  • Up to 50% of patients with dilated cardiomyopathy suffer an episode of VF.
    
  • In hypertrophic cardiomyopathy, unexpected sudden death occurs with reported frequency of up to 3%/yr.
    
• Nonischemic causes of ventricular tachycardia may evolve into VF:
  
  • Drug toxicities (cyclic antidepressants, digitalis)
    
  • Electrolyte or acid–base abnormalities
    
  • Congenital and acquired prolonged QT syndromes.
    
  • Short QT syndrome
    
  • Brugada syndrome
    
• Premature ventricular complexes (PVCs) with R-on-T phenomenon
  
• Other less common causes of VF:
  
  • Electrocution
    
  • Hypoxia
    
  • Hypothermia
    
  • Blunt chest trauma
    
  • Iatrogenic myocardial irritation from pacemaker placement or pulmonary artery catheter
    
• Idiopathic VF (5–10%)