Volume I:
First Thirty Minutes
- Section 1
  Acute Care Algorithm/ Treatment Plans/ Acronyms
- Section 2
  Universal Approach
  - CALS Universal Approach To Emergency Advanced Life Support
- Section 3
  Steps 1-6
- Section 4
  Preliminary Impression/Focused Clinical Pathways
Volume II:
Resuscitation Procedures
Volume III:
Definitive Care

Airway 6: Inspiratory Impedance Threshold Device Portal

I. Use During Resuscitation of Cardiac Arrest Patients

Survival from cardiac arrest is critically dependent on CPR delivering sufficient blood flow to the vital organs to allow for recovery of cardiac function and preservation and restoration of brain function. Even with rapid deployment of EMS in response to cardiac arrest, results of CPR are marginal at best. The reasons for the low resuscitation success rates are many, but include that traditional CPR only provides 10% to 20% of the normal blood flow to the heart and 20% to 30% of normal blood flow to the brain. Thus, CPR frequently cannot provide an adequate blood pressure and vital organ perfusion pressure to restore normal organ function.¹

Much research has been conducted to find a way to enhance vital organ perfusion during CPR. A hypothesis has emerged that by “priming the pump,” by enhancing venous return during CPR, survival after cardiac arrest can be improved.² Two approaches have been discovered to increase venous return to the heart during the decompression or relaxation phase of CPR. These approaches include:

1. Active compression-decompression (ACD) CPR.²During the compression phase, blood is forced out of the heart into the circulation. During the decompression or relaxation phase, the ACD device is pulled up, which creates a vacuum within the chest cavity, and more blood is drawn into the heart to be expelled with the next compression of the chest.

2. An impedance threshold device (ITD) used during CPR.²The ITD is a small (35 mL) device that can be attached to the endotracheal tube, LMA, Combitube™, King Airway, or face mask. Within the ITD is a valve with a diaphragm designed to impede or inhibit passive airflow into the patient’s lungs when the intrathoracic pressure is less than 0 atm (or negative), as occurs during the relaxation phase of normal CPR. This negative intrathoracic pressure is created naturally by the intrinsic elastic recoil of the chest wall that occurs during the decompression or relaxation phase of CPR. The ITD thus maintains a vacuum within the chest cavity that enhances the venous return to the heart and results in an increase in the volume of blood within the heart available to be expelled with the next chest compression during CPR. During ventilation by a rescuer, gas exchange in not impeded by the ITD during either the expiration or inspiration phases of ventilation.²The ITD also does not impede the movement of air out of the chest during chest compression or if the patient begins to breathe on their own. The ITD is removed after the patient returns to spontaneous respirations and circulation.² One such device is the ResQPOD. (See image at left.)

The application of the ITD thus results in a lowering of intrathoracic pressure
during the relaxation phase of standard CPR so as to enhance venous blood
return to the heart and overall CPR efficiency. A negative pressure of -10 cm
water seems to have the maximum effect on facilitating venous return into the
heart and thus improving cardiac output during CPR.³

To help maximize CPR efficiency and the effectiveness of the ITD, complete chest wall recoil must be allowed between chest compressions and the frequency and overall time used for the delivery of breaths must be minimized within some careful parameters. Research suggests that limiting ventilation frequency in an intubated patient receiving CPR to no more than 12 breaths/minute can be beneficial.⁴ Studies suggest that excessive ventilation rates may cause a reduction in coronary perfusion pressures and a reduction in CPR survival.⁴

Hemodynamic benefits of the use of the ITD in patients undergoing standard CPR in human studies include⁵:

Almost 100% increase in systolic blood pressure in the ITD-treated patients vs sham controls^*
A non-statistically significant increase in diastolic blood pressure in the ITD group
A non-statistically significant increase in ETCO_{2 i}n the active ITD group

Clinical outcome studies on the use of the ITD during CPR lack statistically significant long-term survival data. However, increased survival to 24 hours post-arrest is an important surrogate for a successful, long-term benefit²and is stronger evidence than ROSC (Return of Spontaneous Circulation) or hospital admission percentage used to evaluate other newer therapies^.6,7 These include use of amiodarone for the treatment of ventricular fibrillation⁶ and of new defibrillation wave forms.⁷ This evidence on the value of using the ITD during CPR has resulted in its application now being listed as a Class IIA recommendation by the American Heart Association.⁸

Outcome studies available on the use of the ITD during CPR include:

In a pre-hospital study conducted in Staffordshire, UK,⁴ short-term survival (endpoint or outcome being defined as alive with a perfusing pulse on admission to the hospital ED) in patients treated with the ITD was shown to be increased over historical controls. Those receiving ITD treatment had a 50% increase in survival to hospital ED admission (34% with ITD vs 22% [historical controls]). Survival of those presenting with an initial asystolic rhythm was tripled in the group receiving ITD treatment (34% vs 11% [historical controls]).
In a pre-hospital study conducted in Milwaukee, WI, ⁹patients presenting in PEA treated with the ITD had an increased rate of admission to the ICU and increased 24-hour survival vs sham controls (52% vs 20% and 30% vs 12%, respectively; P=0.01). This patient group traditionally has a poor prognosis. In this study, those presenting in ventricular fibrillation or asystole did not have a statistically significant difference between ITD vs sham treatment.
In the Milwaukee study, ⁹ there were too few survivors to hospital discharge to gain a statistically significant trend in assessment of neural outcome. Nevertheless, a trend was observed where, at hospital discharge and 30 days post-discharge, 1 of 4 sham-ITD and 3 of 5 active-ITD patients who survived had normal neurological function.

Conclusion
Studies suggest a trend toward improved survival, at least short-term survival, in patients presenting in cardiac arrest who are treated with the ITD during resuscitation. The ITD is easy to use and easy for rescuers of cardiac arrest patients to learn to use. If used, the ITD should be implemented early in the cardiac arrest resuscitation. This includes use by BLS providers with a face mask, LMA, King Airway, or Combitube™.

Addendum: In the 2010 AHA Guidelines for CPR and Emergency Cardiovascular Care, the impedance threshold device was moved from a Class IIa (reasonable to use) to a Class IIb (may be considered) recommendation.¹⁰ Enrollment in a very large, prospective study conducted by the National Institutes of Health was terminated after several novel interventions, including the use of an ITD, failed to improve survival in over 11 000 victims of out-of-hospital cardiac arrest.¹¹

II. Use in Spontaneously Breathing, Hypotensive Patients

Maintaining adequate vital organ perfusion in patients with severe hypotension where IV access, IV fluids, drug therapy, and/or surgical intervention may not be immediately available is often challenging. This is especially true in cases of hemorrhagic shock as occurs in both civilian and combat trauma.

While the ITD was originally developed to improve circulation during CPR after cardiac arrest, laboratory experiments have demonstrated that applying airway resistance during spontaneous inspiration with the use of an ITD in normovolemic, normotensive persons result in an increase in stroke volume, cardiac output, and systolic blood pressure.¹² Thus, it is logical to consider if there is a potential benefit to the use of the ITD in patients with hemorrhagic or other forms of hypovolemic shock before other lifesaving interventions can be initiated or become effective. ResQGARD is an example of an ITD for use in spontaneously breathing, hypotensive patients. See image below at left.

The physiologic explanation for the anticipated increase in stroke
volume, cardiac output, and systolic blood pressure with the ITD in
hypotensive, spontaneously breathing patients is based on the observation
that normal inspiration causes a decrease in intrathoracic pressure,
which causes the development of a negative pressure in the atria and t
hus an increase in venous return to the heart. By applying an ITD
to the airway of a spontaneously breathing patient, a greater negative
intrathoracic pressure, or a modest vacuum, can be created that
further enhances the venous return to the heart and thus an increase
in the cardiac output and systolic blood pressure.¹³

Experimental studies in animal and human subjects have shown:

In anesthetized, spontaneously breathing domestic piglets made hypotensive by bloodletting of 40% of their blood volume, the application of the ITD into their airway (set at -7 cm of water) resulted in a rapid sustained significantly greater stroke volume, cardiac index, and systolic blood pressure. Specifically, the stroke volume index increased by 42%, the cardiac index by 43%, and the systolic blood pressure by 43%.¹⁴
Experimental hypotension was induced in healthy human volunteers, to simulate loss of central blood volume or hemorrhage, by applying lower body (below the iliac crest) negative pressure induced with an airtight skirt and a vacuum chamber. The attachment of the ITD to a face mask (set at -7 cm of water) applied to the face of a spontaneously breathing subject resulted in an increased blood pressure and delayed the onset of cardiovascular collapse and circulatory shock during severe hypovolemic hypotension.¹³
In a study of patients who experience significant symptomatic postural hypotension, the use of the ITD resulted in a significant reduction in the magnitude of the upright posture-induced symptoms of dizziness, lightheadedness, and “gray out” of vision. This appears to be true when there is either insufficient arterial constriction (ie, inappropriate peripheral arterial dilatation as with relative “autonomic failure”) or with hypovolemia. Both of these situations result in an inadequate venous return to maintain a functional normal blood pressure with upright posture.¹⁵
In a small study of spontaneously breathing hypotensive patients in the ED, the use of the ITD resulted in a rapid increase in systolic blood pressure compared to a sham device used in control patients. The maximum increase in systolic blood pressure was 12 ± 8 mmHg with the active ITD vs 5 ± 6 mmHg with the sham device (P<0.01).¹⁶

Use of the ITD for the initial management of hypotension secondary to hypovolemia includes the following theoretical advantages:

Does not require intravenous access¹⁴
Does not require the immediate availability of drugs or blood replacement treatments¹⁴
Does not dilute the clotting factors and RBC concentration of the patient’s blood¹⁴
May buy some time to obtain IV access, obtain and give needed blood products, and deliver definitive treatment aimed at the cause of the hypovolemic hypotension¹⁴
May be a lifesaving intervention when used in patients suffering from life-threatening hemorrhage¹³

Some potential risks or difficulties to the use of the ITD in hypotensive, spontaneously breathing patients include:

In patients who have experienced severe hemorrhage, it is possible that the increase in blood pressure induced by the use of the ITD may exacerbate the bleeding or dislodge hemostatic clots that have spontaneously formed. This may cause an increase in bleeding and further depletion of blood volume and clotting factors.¹³
There are some hypovolemic, hypotensive patients where the use of the ITD does not seem to be helpful in raising the systolic blood pressure. This may result from ineffective breathing mechanisms by the patient so there is not the development of a therapeutic negative intrathoracic pressure with the use of the ITD.¹³
Patients with very low respiratory rates or rapid shallow breathing may not gain any value from the use of the ITD and thus probably should not have the ITD applied.¹³
Patients who may feel claustrophobic may not tolerate breathing through the ITD.¹⁶
In patients requiring 100% positive pressure ventilation (PPV) but not chest compressions, the ITD will not have any therapeutic benefit. Nevertheless, it does not seem to cause any harm when used with 100% PPV, and it may have some benefit in those patients who have some spontaneous respiratory effort.¹³

The ITD needs to be used with great caution or not at all in some cases. These situations include:

If there is active bleeding, the increase in blood pressure induced by the use of the ITD may increase the blood loss and result in further loss of RBC and clotting factors with further reduction in blood volume. Aggressive attempts must be made to stop the bleeding in all cases of hemorrhage. The lack of control of major hemorrhage may be a relative contraindication to the use of the ITD.
Rapid, shallow, or very slow spontaneous respirations may make the use of the ITD impractical.
If 100% PPV is required, the ITD is unlikely to be of any value unless chest compressions are also required.

Conclusion
The use of the ITD in spontaneously breathing patients with hypovolemic hypotension may augment venous return to the heart and improve the stroke volume and systolic blood pressure. In select patients, this may be of value and help prevent cardiovascular collapse until definitive treatment of the cause for the hypotension can be accomplished.

References

Yannopoulos D, Aufderheide TP, Gabrielli A, et al. Clinical and hemodynamic comparison of 15:2 and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation. Crit Care Med. 2006;34:1444-1449.
Plaisance P, Lurie KG, Vicaut E, et al. Evaluation of an impedance threshold device in patients receiving active compression-decompression cardiopulmonary resuscitation for out of hospital cardiac arrest. Resuscitation. 2004; 61:265-271.
Babbs CF, Yannopoulos D. A dose-response curve for the negative bias pressure of an intrathoracic pressure regulator during CPR. Resuscitation. 2006; 71:365-368.
Thayne RC, Thomas DC, Neville JD, Van Dellen A. Use of an impedance threshold device improves short-term outcomes following out-of-hospital cardiac arrest. Resuscitation. 2005;67:103-108.
Pirrallo RG, Aufderheide TP, Provo TA, Lurie KG. Effect of an inspiratory impedance threshold device on hemodynamics during conventional manual cardiopulmonary resuscitation. Resuscitation. 2005;66:13-20.
Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med. 1999;341:871-878.
Schneider T, Martens PR, Paschen H, et al. Multicenter, randomized, controlled trial of 150-J biphasic shocks compared with 200- to 360-J monophasic shocks in the resuscitation of out-of-hospital cardiac arrest victims. Circulation. 2000;102:1780-1787.
ECC Committee, Subcommittees and Task Forces of the American Heart Association. 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2005;112(24 Suppl):IV1-203.
Aufderheide TP, Pirrallo RG, Provo TA, Lurie KG. Clinical evaluation of an inspiratory impedance threshold device during standard cardiopulmonary resuscitation in patients with out-of-hospital cardiac arrest. Crit Care Med. 2005;33:734-740.
ECC Subcommittee, Subcommittees, and Task Forces of the American Heart Association. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18 suppl 3):S 722.
US Department of Health and Human Services. National Institutes of Health. NHLBI stops enrollment in study on resuscitation methods for cardiac arrest. NIH News. November 6, 2009. http://www.nih.gov/news/health/nov2009/nhlbi-06.htm. Accessed August 22, 2011.
Convertino VA, Ratliff DA, Ryan KL, et al. Hemodynamics associated with breathing through an inspiratory impedance threshold device in human volunteers. Crit Care Med. 2004;32:S381-S386
Convertino VA, Ryan KL, Rickards CA, et al. Inspiratory resistance maintains arterial pressure during central hypovolemia: implications for treatment of patients with severe hemorrhage. Crit Care Med. 2007;35:1145-1152.
Marino BS, Yannopoulos D, Sigurdsson G, et al. Spontaneous breathing through an inspiratory impedance threshold device augments cardiac index and stroke volume index in a pediatric porcine model of hemorrhagic hypovolemia. Crit Care Med. 2004;32:S398-S405.
Melby DP, Lu F, Sakaguchi S, Zook M, Benditt DG. Increased impedance to inspiration ameliorates hemodynamic changes associated with movement to upright posture in orthostatic hypotension: a randomized blinded pilot study. Heart Rhythm. 2007;4:128-135.
Smith SW, Metzger AK, et al. Use of an impedance threshold device in hypotensive patients in the emergency department. Circulation. 2006; 114 (suppl II):18.

Airway 6: Inspiratory Impedance Threshold Device Portal

References

Edition 13-October 2011