Hypotensive patients, like those experiencing shock or, in extreme cases, cardiac arrest, require enhanced blood flow to provide sufficient oxygen to vital organs. Poor perfusion results in poor survival and compromised neurological function. One way to improve outcomes is to regulate negative intrathoracic (chest) pressure by using intrathoracic pressure regulation (IPR)–an innovative therapy that leverages the body’s own physiology.
IPR enhances blood circulation, improves cardiac output and lowers intracranial pressure (ICP) noninvasively to provide better perfusion to the brain. In this article, we’ll explore in detail the physiology behind IPR and its use with hypotensive and cardiac arrest patients.
Physiology & Basic Scientific Evidence
The human body is continually regulating circulation of blood by using positive and negative pressures inside the thoracic cavity. This regulation acts like a bellows. During inhalation, the diaphragm moves down and the chest wall moves out, which creates a negative pressure (or vacuum) that draws air into the lungs and blood into the chest, and slightly lowers ICP. During exhalation, the diaphragm moves up and the chest wall moves in. This creates a positive pressure that forces air out of the lungs, diminishes blood return to the chest and slightly raises ICP.
In addition to moving air, intrathoracic pressure affects blood flow. It is well understood that respiration and circulation are inextricably linked. As far back as 1967, an inverse relationship between intrathoracic pressure and blood flow was observed. Moreno et al showed that as intrathoracic pressure decreases, blood flow back to the heart increases.1 Results from experiments conducted using an animal hemorrhage model support the concept that reduced intrathoracic pressure results in a lowering of right atrial pressure, which in turn pulls more venous blood back into the thorax and increases arterial pressure and cerebral perfusion. This hydraulic effect is shown in Figure 1 (See below.)2
Impact of IPR on blood pressures2
Figure 1: Results from experiments conducted using an animal hemorrhage model support the concept that reduced intrathoracic pressure results in a lowering of right atrial pressure, which in turn pulls more venous blood back into the thorax and increases arterial pressure and cerebral perfusion.
In a healthy person, the body’s normal compensatory response regulates intrathoracic pressure to influence blood pressure. Under stress, such as during exercise, a person breathes harder, faster and deeper. These enhanced pressures in the thoracic cavity help to improve circulation. However, sometimes the body is unable to adequately compensate. For example, in a shock patient, the heart rate increases in an effort to maintain sufficient blood flow, and intrathoracic pressure is modulated in an effort to increase perfusion.3
If the cause of the shock is not corrected, eventually the patient will decompensate and blood pressure will fall. This results in insufficient perfusion to protect the brain and other vital organs.
How IPR Therapy Works
IPR can help patients who are no longer able to compensate for reduced blood flow. Figure 2 (see below) summarizes how this works. IPR enhances the negative pressure in the chest, pulling more blood back to the heart (i.e., increasing preload), which results in increased cardiac output. And because pressures in the chest are also transmitted to the brain, IPR also lowers ICP, which decreases resistance to forward blood flow and makes it easier to get blood to the brain. The net result is improved perfusion to the brain and other vital organs.
Figure 2: IPR Therapy enhances negative intrathoracic pressure, which lowers ICP, increases pre-load and cardiac output, and increases blood flow to the brain.
Another way to think about IPR Therapy is to contrast it to continuous positive airway pressure (CPAP). IPR works in the opposite manner as CPAP, which instead generates positive intrathoracic pressure by forcing air into the lungs.
Used to treat patients with pulmonary edema, CPAP employs positive pressure to drive unwanted fluid out of the lungs. CPAP’s positive pressure ventilation therefore has an opposing effect on the cardiovascular system as compared to IPR: CPAP decreases cardiac output and blood pressure, while IPR Therapy increases these physiological parameters. (See Figure 3 below.)
Comparison of positive and negative pressure therapies
Figure 3: We use positive pressure therapies (e.g., CPAP) to push fluids and air out, while negative pressure (e.g., IPR) can be used to draw fluids and air back to the chest.
IPR Therapy is currently delivered through impedance threshold devices (ITDs) which have mechanisms to enhance the negative pressure in the chest. This greater vacuum draws more blood into the chest and also lowers intracranial pressure, resulting in more perfusion to the brain and vital organs.4
The primary function of an ITD is to improve circulation by enhancing negative intrathoracic pressure. Data from clinical and preclinical studies support the notion that ITDs enhance negative intrathoracic pressure in both cardiac arrest and hypotensive patients.
- During active compression decompression CPR (ACD-CPR), an ITD lowered intrathoracic pressures from -1 mmHg (sham ITD) to -5 to -7 mmHg (active ITD) in out-of-hospital cardiac arrest patients in a randomized, double-blinded, prospective clinical trial.5
- In a study conducted using humans subjected to a simulated hemorrhage of 30%, peak negative intrathoracic pressure was negligible with a sham ITD, but decreased to -12 cmH2O when an active ITD was applied.6
Data on the use of ITDs to deliver IPR is extensive. More than 50 animal and human studies have been conducted on the use of ITDs in both conventional and ACD-CPR, and more than 30 animal and human studies have been published on the use of an ITD in improving hemodynamics during shock from a variety of etiologies.
How an ITD Works in Hypotensive Patients
The ITD works in spontaneously breathing patients with low blood pressure by creating a slight amount of therapeutic resistance during inhalation. (See Figure 4 below.) This resistance enhances negative intrathoracic pressure, which in turn improves perfusion to the brain and other vital organs. An ITD is simple to use and can be applied by all levels of rescuers. With or without intravascular fluids, studies have shown that use of the ITD increases systolic and diastolic blood pressures by up to 30%.6
The ITD 7
Figure 4: IPR is delivered by the ITD 7 for spontaneously breathing hypotensive patients.
However, an ITD has advantages over fluids in that it is non-invasive, it does not dilute clotting factors, and it does not cause spikes in blood pressure that may be associated with “popping the clot,” thus complementing a permissive hypotensive approach to blood pressure management.8,9 Supplemental oxygen may also be administered through the device.
Clinical and experimental studies on use of the IPR in hypotension have shown many benefits:
- In a pre-clinical study, use of an ITD increased cardiac output by nearly 25% during a reduction of >50% in central blood volume.10
- The ITD improved systolic blood pressure (SBP) by 25% to 30% during prehospital treatment of hypotensive patients.7,11
- Use of an ITD allowed for permissive hypotension in a recent clinical study.11
- Application of IPR Therapy results in improved oxygen delivery to the brain, which is frequently associated with an improved feeling of well-being in severely hypotensive patients during prehospital care.2,12
Use of an ITD has also been shown to extend the window of treatment for shock patients. In a laboratory experiment designed to simulate continuous progressive hemorrhage in humans, use of an ITD increased the time to cardiovascular collapse (decompensatory shock) by an average of 44%.6
In two studies conducted at independent sites, use of an ITD was shown to be effective in elevating blood pressure in hypotensive patients (~78/50 mmHg) during prehospital care, while still maintaining permissive hypotension (100/65 mmHg).7,11 After application of the ITD, a 47% increase in pulse pressure and improved feelings of well-being were reported in >85% of the patients, which is consistent with mechanisms of increased stroke volume and cerebral perfusion. We will explore the use of an ITD in hypotension in another article in this supplement.
How an ITD Works During CPR
Even when performed well, conventional CPR provides only about 25% of normal blood flow to vital organs.13 This inadequate perfusion of tissues is due in part to an inherent inefficiency of CPR that impacts preload. As the chest wall recoils during CPR, a slight negative pressure (vacuum) develops in the chest that refills the heart. Since the victim’s airway is open, air flows freely into the lungs and neutralizes the vacuum that is responsible for creating preload.
The ITD can be used in patients with low blood flow who are not spontaneously breathing (e.g., those patients in cardiac arrest undergoing CPR). It is placed into the ventilation circuit, and when used in combination with CPR, it prevents unnecessary air from flowing into the victim only during the chest wall recoil phase. (See Figure 5 below.)
The ITD 10
Figure 5: IPR is delivered by the ITD 10 for patients in cardiac arrest. The ITD can be used on a face mask or advanced airway.
If the body cannot draw air in, it instead pulls more blood back to the chest, increasing preload, as it attempts to equalize the vacuum. Patient ventilation and exhalation are not compromised in any way, and a safety check will open at -10 cmH2O should the patient begin to breathe or gasp. Timing assist lights may be turned on to guide proper chest compression and ventilation, thus promoting high-quality CPR.
Studies on the use of IPR during CPR have shown increased blood flow to the heart and brain. Evidence has also shown that when an ITD is used in conjunction with ACD-CPR, which optimizes chest wall recoil, blood flow is even further enhanced.14
Key findings from clinical trials showed:
IPR increased systolic blood pressure (SBP) compared to standard CPR (an 85% increase in SBP after 14 minutes of IPR use) in a small, prospective, double-blind study in out-of-hospital cardiac arrest patients randomized to IPR versus a sham control.15
- Near-normal blood pressures were obtained when an ITD was used in conjunction with an ACD-CPR device in human subjects.16
- In addition, several pre-clinical trials have shown (note that pre-clinical results may not be indicative of clinical results):
- IPR significantly increases cardiac output compared to standard CPR. In a basic science study of nine pigs, cardiac output increased by 57% using IPR as compared to standard CPR.17
- A pre-clinical study showed IPR increased global brain blood flow by 27% compared to standard CPR.18
- Mean carotid blood flow increased by 37% using IPR as compared to standard CPR in a pre-clinical study.17
Multiple studies using ITDs have demonstrated improved outcomes from cardiac arrest. One study showed that ACD-CPR with an ITD improved 24-hour survival by 45% compared to ACD-CPR alone.19
An even larger prospective, randomized, controlled study showed that long-term survival improved by 49% in adult patients with non-traumatic cardiac arrest who received the combination of an ITD with ACD-CPR vs. standard CPR.20
Conclusion
Intrathoracic pressure regulation (IPR) helps the body help itself in cardiac arrest and shock, and is uniquely designed to improve cerebral perfusion. Animal and human studies have shown that IPR enhances vital organ circulation and outcomes in both hypotensive and cardiac arrest patients.
More Cardiac Care from JEMS.com.
References
1. Moreno AH, Burchell AR, Van der Woude R, et al. Respiratory regulation of splanchnic and systemic venous return. Am J Physiol. 1967;213(2):455—465.
2. Convertino VA et al. Optimizing the respiratory pump: Harnessing inspiratory resistance to treat systemic hypotension. Respiratory Care 2011;56(6):846-57.
3. Shoemaker WC, Montgomery ES, Kaplan E, et al. Physiologic patterns in surviving and nonsurviving shock patients. Use of sequential cardiorespiratory variables in defining criteria for therapeutic goals and early warning of death. Arch Surg. 1973;106(5):630—636.
4. Aufderheide TP, Alexander C, Lick C, et al. From laboratory science to six emergency medical services systems: New understanding of the physiology of cardiopulmonary resuscitation increases survival rates after cardiac arrest. Crit Care Med. 2008;36(11 Suppl):S397—404.
5. Plaisance P, Soleil C, Lurie KG, et al. Use of an inspiratory impedance threshold device on a facemask and endotracheal tube to reduce intrathoracic pressures during the decompression phase of active compression-decompression cardiopulmonary resuscitation. Crit Care Med. 2005;33(5):990—994.
6. 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(4):1145—1152.
7. Convertino VA, Parquette B, Zeihr J, et al. Use of respiratory impedance in prehospital care of hypotensive patients associated with hemorrhage and trauma: a case series. J Trauma Acute Care Surg. 2012;73(2 Suppl 1):S54—59.
8. Smith SW, Parquette B, Lindstrom D, et al. An impedance threshold device increases blood pressure in hypotensive patients. J Emerg Med. 2011;41(5):549—558.
9. Metzger A, Rees J, Segal N, et al. “Fluidless” resuscitation with permissive hypotension via impedance threshold device therapy compared with normal saline resuscitation in a porcine model of severe hemorrhage. J Trauma Acute Care Surg. 2013;75(2 Suppl 2):S203—209.
10. Lurie KG, Zielinski TM, McKnite SH, et al. Treatment of hypotension in pigs with an inspiratory impedance threshold device: a feasibility study. Crit Care Med. 2004;32:1555-1562.
11. Wampler et al. Use of an impedance threshold device in spontaneously breathing patients with hypotension secondary to trauma: an observational cohort feasibility study. J Trauma Acute Care Surg. 2014; 77(3 Suppl 2):S140-S145.
12. Rickards CA, Ryan KL, Cooke WH, et al. Inspiratory resistance delays the reporting of symptoms with central hypovolemia: association with cerebral blood flow. Am J Physiol Regul Integr Comp Physiol. 2007;293(1):R243—250.
13. Andreka P, Frenneaux MP. Haemodynamics of cardiac arrest and resuscitation. Curr Opin Crit Care. 2006;12(3):198—203.
14. Voelckel WG, Lurie KG, Sweeney M et al. Effects of active compression-decompression cardiopulmonary resuscitation with the inspiratory threshold valve in a young porcine model of cardiac arrest. Pediatr Res. 2002;51(4):523—527.
15. Pirrallo RG, Aufderheide TP, Provo TA, et al. Effect of an inspiratory impedance threshold device on hemodynamics during conventional manual cardiopulmonary resuscitation. Resuscitation. 2005;66(1):13—20.
16. Plaisance P, Lurie KG, Payen D. Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation: a randomized evaluation in patients in cardiac arrest. Circulation. 2000;101(9):989—994.
17. 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(5):1444—1449.
18. Lurie KG, Voelckel WG, Zielinski T, et al. Improving standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve in a porcine model of cardiac arrest. Anesth Analg. 2001;93(3):649—655.
19. 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(3):265—271.
20. ResQCPR System: Sponsor Executive Summary. (May 6, 2014.) Food and Drug Administration. Retrieved Oct. 15, 2014, from www.fda.gov/downloads/AdvisoryCommittees/CommitteesMeetingMaterials/MedicalDevices/MedicalDevicesAdvisoryCommittee/CirculatorySystemDevicesPanel/UCM395644.pdf
