5. Compression
• Increased intrathoracic pressure
• Ejects blood from heart and lungs
• “Good” compression increases
forward output and BP
Decompression (recoil)
• Decreased intrathoracic pressure
• Refilling of heart and lungs
• “Good” recoil vacuum
refilling forward output
6. Decompression
(“diastole”)
Criley JM et al. Circulation 1986;74(IV):42-50.
Compression
(“systole”)
Hemodynamics of CPR
RT ATRIUM
Aorta
RT ATRIUM
Organ perfusion
LEFT VENTRICLE
Heart + organ perfusion
EXTRATHORAIC VEINS
60
40
0
mm Hg
7. Coronary Perfusion Pressure and ROSC in Human CPR
Paradis NA., et al. JAMA 1990;263:1106-1113
*CorPP = Aorta – RA pressure gradient during relaxation (diastolic) phase of precordial compression
15-19
0-14
20-24
25-39
40-45
36%
57%
50%
100%
80%
0%
ROSC
n=24 CorPP 25.6±7.7 mm Hg
No ROSC
n= 76 CorPP 8.4±10 mm Hg
n=100 patients with
cardiac arrest
55+ (normal)
Coronary
perfusion
pressure
(CorPP)
Coronary
perfusion
pressure
(CorPP)
8. Edelson DP et al. Resuscitation 2006;71:137-45
• n = 60 consecutive VF resuscitations/shock
− 63% men, 65 y/o
− Time to 1st shock = 3.7min
• Measurements
− Compression depth = mm during 30 sec before 1st shock
• Outcomes
− Successful shock = VF terminated ≥ 5 sec
− ROSC = organized rhythm/pulse/BP ≥ 20 min
9. Edelson DP et al. Resuscitation 2006;71:137-45
Effect of CC Depth on Shock Success
ORadj*1.99/↑5 mm compression depth (95%CI 1-08-3-66, p=0.028)
*Arrest location, age, sex, time-to-shock
AHA recommendations 1.5-2” (4-5 cm)
†
†
13. Wik L et al JAMA 2005;293:299-304
• n=176 adults with out-of-hospital cardiac arrest
• Automated resuscitation monitoring
– Compression rate, depth, “hands off” time
– Ventilation rate
– ECG
– Events
14. Quality of CPR During Out-of-
Hospital Cardiac Arrest
Wik L et al JAMA 2005;293:299-304
n=176
Vs AHA Guidelines
chest compression
100 ± 10/min
(75 @ 30:2)
Vs AHA Guidelines
compression depth
38-52 mm (1.5-2”)
60
25
64
23
35
10
34
9
*Average # compressions given per minute vs instantaneous rate at which
compressions, when given, were administered (120 20)
*
49%
21
48%
18
† % time without spontaneous circulation or
chest compressions
†
~12%
@ 30:2
15. Yu T et al. Circulation 2002;106:368-372
• 20 instrumented swine
• 7 minutes of unsupported VF
CPR + AED
“Hands-off” interval prior to each shock
(mimicking analysis and charge interval of AEDs (10-19secs))
3 secs 10 secs 15 secs 20 secs
16. Yu T et al. Circulation 2002;106:368-372
Effect of Interrupted Precordial Compression
on Resuscitation Outcome
100%
80%
40%
0
Successfully Resuscitated
Seconds of Interrupted CPR
n=5 per group
p<0.05 p<0.01
p<0.05
17. • n=9 instrumented swine
• 6 minutes untreated VF standard CPR* x 3 min CPR with 75%
recoil (residual 1.2 cm sternal compression @ end decompression)
x 1 min standard CPR* x 1 min defib x 3 ACLS
Yannopoulos D et al. Resuscitation 2005;64:363-72
*Standard CPR = CC @100/min, 50% duty cycle, 5 cm depth, full (100%) recoil, 15:2 ratio
18. Effect of Incomplete Chest Decompression
On Coronary and Cerebral Perfusion Pressures
†(MAP – mean ICP pressure)
*(Ao Diastolic-RAP)
p<0.05
p<0.05
mm
Hg
% Chest recoil
Yannopoulos D et al. Resuscitation 2005;64:363-72; Paradis et al JAMA 1990;263:3257-8
n=9 instrumented swine std CPR (100% recoil) x 3’ CPR (75% recoil) x 1’
* †
Critical pressure for ROSC
*†
*
†
*†
*
*
*
19. Percent Survival from
Witnessed VF Rhythm
Importance of High-Performance
Resuscitation
35%
0
10
20
30
40
50
60
2000 - 2004 2005 - 2009
percent
survival
48%
New Protocol
20. Take home points
• Quality of CPR is critical
– Rate
– Depth
– Recoil
• High Density CPR (also ‘high performance CPR’)
– Achieved with a carefully choreographed approach
– Chest compressions must occur 90% of the time
21. Annual Utstein Survival for
Chelan/Douglas Counties
30.0%*
41.7%
53.8%
0%
10%
20%
30%
40%
50%
60%
2010 2011 2012
*Incomplete data for 2010
Editor's Notes
Dr Kudenchuk is a cardiologist with UW medicine. He has been very involved in the Resuscitation Academy.
Only 2 pre-hospital interventions have clearly been shown to improve survival: chest compressions and defibrillation. We want to maximize our ability to perform these interventions.
Seattle has been monitoring their survival rates for OHCA since the mid 70’s. Here we see the survival rate for those with VF on arrival of the fire department. In 1984, AEDs were placed on over 50% of the fire engines. By 1990, all first responders had AEDs. One would expect that survival would increase, but that is not what was observed. Why? One hypothesis, was that responders were focusing on the AED to the neglect of quality CPR.
What would happen if they had first responders perform CPR first, before shocking, even if the rhythm was shockable?
In 1994 they started ‘CPR first’. They then compared this with the 4 years prior when ‘shock first’ was the protocol. These were all patients with a shockable rhythm on first contact. They then compared them by response interval. You can see that if the response was 2 minutes or less, shock first was as good as, or even better (2minutes) than ‘CPR first’. However, after 2 minutes, there was a sustained improvement in survival with the ‘CPR first’ group, even though, as expected, survival would diminish with the increasing response time.
Question: So why might CPR first be important in improving survival? Then begin overview of what CPR actually does on the subsequent slides
Two phases of compressions. Have people thinking about what compressions actually do. It is more than just the heart…down compression affects the entire chest (thoracic) cavity.
The recoil phase then creates negative pressure, which pulls blood back into the thoracic cavity (including the heart). Have people think about the logical consequences of poor recoil: inadequate filling of the heart means less blood pushed out with compression and therefore decreased pressure.
This may be the most complicated slide. Spend plenty of time on it so people understand the concepts. These concepts are key to understanding what we’re trying to achieve.
Begin by discussing the left ventricular pressure tracing through compression and decompression. Then follow aortic pressures. Ask the question, ‘Why does aortic pressure not drop as low as ventricular pressure in diastole?” The answer is the aortic valve, which closes and maintains some pressure there. Next, follow the right atrial tracing. It nearly mimics the left ventricular tracing, which only occurs during CPR when the pressures exerted on the heart are equal in all 4 chambers. Then discuss coronary artery flow. People may know the coronaries begin at the aortic root, but often don’t realize that the coronary veins empty into the right atrium. Ask where they empty into? Then follow the right atrial pressures. Then emphasize the difference between aortic and atrial pressures in diastole (decompression). I like to get people to think about a pressure system, where flow will only occur from an area of higher pressure , to one of lower pressure. So this pressure difference is what allows for coronary blood flow. Point out there can be no flow in the compression phase. So coronary perfusion pressure is developed in the decompression phase. So when performing compressions, one can think about the compression phase as perfusing the brain, and the decompression phase as perfusing the heart. “Brain—Heart—Brain—Heart—Brain—Heart”
Make sure everyone understands this!
This slide is the graphic presentation of 100 patients monitored in an ICU who developed cardiac arrest. Because of invasive monitoring, they were able to measure coronary perfusion pressure (CPP). On the graph on the left, you can see there was no ROSC if CPP was less than 15. Furthermore, there is a clear trend towards improved likelihood of ROSC when CPP is increased. On the right are two graphs showing actual data for two of the patients; one without and one with ROSC. The top graph shows measured aortic pressure while the middle shows measure right atrial pressures. One can see that there was no difference between the two and so CPP was about 0. In fact, 76 patients had no ROSC and their mean CPP was 8.4. On the other patient (far right graph) one can see there is a difference between aortic and right atrial pressures during diastole (decompression). Decompression aortic pressure is 40, while decompression right atrial pressure is 20. So there is a CPP of about 20 (above that critical threshold of 15). In fact, in the 24 patients who achieved ROSC, the mean CPP was 25.6. Emphasize that generating a high CPP is absolutely critical in achieving ROSC.
This study looked at people with VF arrest. They measured compression depth in the 30 seconds before the 1st shock. The outcome measure was a successful shock defined as terminating VF for at least 5 seconds. A secondary outcome was ROSC (with pulse and BP) for at least 20 minutes.
This graph clearly shows a relationship between compression depth and shock success. Note the old AHA recommendation (prior to 2010) was 39-50mm. Now it is >50mm or 2 inches. In those patients, shock success occurred 100% of the time.
This tracing shows Aortic and RA pressures during chest compressions. Note CPR “systole” and “diastole”. This shows that it takes time to develop adequate CPP…it doesn’t just happen as soon as you start compressions. In fact, this tracing shows it taking 30 compressions, or 16 seconds. Then, notice how quickly that hard earned CPP is lost when there is a pause in CPR…only 3 seconds. There is a price to be paid every time you pause.
This was a study asking paramedics and EMTs if they could correctly perform each of these aspects of chest compression. Most, of course, thought they could do this correctly. So then they had these same folks perform CPR and measure these different aspects. Here are the results…
Reality didn’t quite meet up to perceptions. Notice the abysmally low percentages for the critical components of recoil and depth. We need to measure ourselves and see what we’re doing well, and improve on those things we’re not doing well in.
This study looked at 176 OHCA patients with automated monitoring of various aspects, including compression rate, depth and “hands off” time.
They measured in over the 1st 5 minutes as well as the entire episode. One can see the low compression rate (see the fine print) as well as poor compression depth. And finally, near 50% of the time, there were no compressions being done. This is due to various things such as pulse checks, IV’s, intubation, rhythm interpretation, poor coordination. What other factors might stop compressions?
This is a pig study (bacon jokes are Kosher! Ha). They took 20 monitored pigs and put them into VF. The investigators gossiped and drank coffee for 7 minutes. Then they started CPR. Before providing a shock, they determined a ‘hands off’ period to mimic charging of the defibrillator. The hands off periods were predetermined to be 3, 10, 15 and 20 seconds. Was there any difference in shock success when comparing these different groups?
Clearly, the longer the compression pause prior to shock, the lower the likelihood of success. No pigs survived in the 20 second pause group.
This was another pig study. They took 9 pigs and put them into VF and did nothing for 6 minutes. Then they started standard CPR (this was based on 2000 AHA guidelines…see *). After 3 minutes of standard CPR they changed one thing. They changed the recoil to be only 75% instead of 100% recoil. They did that for 1 min then changed back to standard CPR for 1 more minute.
One can see that with the standard CPR, CPP pressure was adequate. However, when just the recoil was reduced to 75%, the CPP dropped below that critical threshold of 15mm Hg. The interesting piece, is that when standard CPR was resumed, CPP improved, but not anywhere close to where it had been. This was also true for cerebral perfusion pressure. It is important to maintain quality compressions throughout the resuscitation.
In 2005, Seattle introduced a new protocol with an emphasis on eliminating pauses in compressions. Procedures, including intubation, were not to interfere with compressions. They improved there compression percentage to over 90%. There was a dramatic improvement in survival to hospital discharge.
2011 marked the first time data was collected on OHCA outcomes. 2010 numbers come from a retrospective review of data. Patients transported to the hospital were over represented, so actual survival in 2010 was probable less (witnessed VF arrests called in the field were probably missed when looking back at the data). So this program has clearly improved survival in Chelan and Douglas Counties.
