EMCrit.org

Adult Resuscitation

Incredible Review (DM=Disease-A-Month 1997;July:433)

Bobrow's Review

Myocardial blood flow is 25% normal, cerebral blood flow is 50% normal during well performed CPR

because outflow is low, much smaller amounts of ventilation are needed to maintain normal V/Q ratios. Emphasis should always be on consistent compressions with a de-emphasis on breathing

Huge difference in the PaCO2 and PvCO2. alkalemic in arteries and hypercarbic in veins

Palpating pulses during CPR has poor correlation with actual flow, it just represents pressure transmission to the arteries (DM)

A complete balloon occlusion of aorta still allows pulses to be palpated. ETCO2 or amplitude of V-Fib are more predictive (DM)

Survival decreases 5-10% for every minute of arrest, though this may not be linear

As CPR goes on, it becomes less effective due to changes in heart and chest compliance

ETCO2 predictive of success (Crit Care Med 1985, 13:907)

>10 indicates potential survival (NEJM 1988 318:607 & JAMA 1989 262:1347 & Ann Emerg Med 1995;25:762-767)

ETCO2 <10 at 20 minutes in a PEA code--no chance of survival (NEJM 1997;337:301-6)

If arrest time is <6 minutes then code for 30 minutes; If arrest time is >6 minutes, code for 15 minutes (Crit Care Med 1985,13:930-931)

Coma that persists longer than 4 hours after CPR predicts a poor prognosis for full neuro recovery

Absence of pupillary light reflex after 24 hours indicates little or no chance for neuro recovery (Marino)

Pulse with compressions is not helpful (Circ 2000 102:I86)

ILCOR statement on hypothermia after out of hospital arrest with return of spontaneous circulation 32-34 C for 12-24 hours then slow rewarming. (Resus 2003, 57:231)

1. The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. New England Journal of Medicine. 2002;346:549-56.

2. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, Smith K. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. New England Journal of Medicine. 346(8):557-63, 2002.
 

Get Venous Blood Gas, not arterial as this is more representative of systemic oxygenation (Marino)

Vasopressin in Asystole (NEJM 350(2), Jan 8 2004)

40 U IV Q3 x 2 doses, then switch to Epi 1 mg Q 3-5 minutes

 

 

 

Figure 1: Probability of survival without severe neurological deficit as a function of time following cardiac arrest

ACLS Guidelines

ACLS 2000 guidelines

2005 Guidelines

• Push Hard (Adequately compress the chest) and
• Push Fast (100 per minute)

Allow Chest to recoil completely after each compression.

A new ratio of compressions to ventilations has been established for one and two rescuer CPR:
30 Compressions to 2 Ventilations (this is considered 1 cycle)

Ventilations should be given over ~1 second; they should be sufficient to just cause chest rise.
The detrimental effects of hyperventilation are emphasized.

ACLS

The most striking change to ACLS is again, the stressing of the importance of well-performed, continuous chest compressions. To this end, all interruptions of compressions are limited. Any interruptions should take less than 10 seconds.

Sequencing:
Perform the initial ABCs as we always have.

Perform CPR until an AED or manual defib is available.

If V-Fib or V-tach is present, administer a
Single Shock at 360 J (for monophasic defibs. Biphasics should have a device-specific, single energy setting picked by maker)
Do not perform a pulse check, but instead immediately restart CPR for 5 cycles (~2 minutes)
Now perform a rhythm check; only check pulse if there is an organized, possibly perfusing rhythm.
If still v-fib/v-tach, shock again at 360 J
Follow this with another 2 minutes of CPR
 

Just to reiterate:
No more 200 or 300 J shocks.
No more stacked shocks
No more interrupting CPR for extended pulse checks.
CPR – RHYTHM CHECK – CPR (while charging) – SHOCK sequence (repeated as needed).

The only interruptions to CPR should be advanced airway placement, rhythm checks, or defibrillations.

Plan all interventions around effective CPR!

CPR should be restarted between the time of identification of a shockable rhythm and the charging/preparation of the defib.

Rhythm checks should occur every 2 minutes (remember, no pulse check unless an organized rhythm is seen.) This same 2 minute mark also should be used to change the provider performing compressions. The quality of compressions starts to suffer at this point, even if the stoic person slamming on the chest does not want to admit it.

Ventilations
Continue 30:2 until advanced airway placed
With airway in place, ventilations are asynchronous at 8-10 per minute

Drugs
Give drugs IV or IO, ET route is allowed, but deemphasized and preferably avoided
Give drugs during CPR immediately following rhythm check, have them prepared prior to the rhythm check

Start EPI after the second shock
Give Epi 1 mg every 3-5 minutes

Vasopressin may take the place the 1st or 2nd epi dose in V-Fib/V-Tach/Asystole, but this is deemphasized due to lack of good evidence.

If still in V-Fib/V-Tach, give antidysrhythmics after the third shock, Amio if available; lido if not. Magnesium for torsades.

PEA/Asystole

These two have been combined into 1 algorithm.

Major differences are hypoglycemia and elevated ICP have been added to the mnemonic of reversible causes.
These contributing factors are referred to as the H’s (hypovolemia, hypoxia, hydrogen ion, hypo-/hyperkalemia, hypoglycemia, hypothermia) and T’s (toxins, tamponade, tension pneumothorax, thrombosis [includes MI or pulmonary embolus], trauma [hypovolemia or elevated ICP]).

Thrombolytics

"There is insufficient evidence to recommend for or against
the routine use of fibrinolysis for cardiac arrest. It may be
considered on a case-by-case basis when pulmonary embolus
is suspected (Class IIa). "

New Metaanalysis

Resus 2006;70:31

8 papers

Lytics increased ROSC, 24 hr survival, discharge, neuro function, and severe bleeds. All bleeds were treatable. Since the bleeding rate was only recorded in survivors, it may just be that rate is the same in both groups but only treatment bleeds seen.

Impedance Threshold Device (ITD)

Although increased long-term survival rates have not been
documented, when the impedance threshold device (ResQValve, Advanced Circulatory Systems) is used by trained personnel as an adjunct to CPR in intubated adult cardiac arrest patients, it can improve hemodynamic parameters and ROSC (Class IIa).

Inspiratory Impedence Threshold Valves (ITVs) are devices attached to resuscitation breathing circuits that prevent passive indrawing of air during chest recoil/decompression following chest compression as part of CPR. In doing so the ITV enhances the period of negative intrathoracic pressure thereby augmenting venous return and so improving CPR-generated cardiac output.92 ITVs are particularly effective when combined with active compression–decompression CPR (ACD CPR) but also provide some benefit during conventional CPR.93 and 94 In order for the ITV to be effective a negative intrathoracic pressure must be maintained.

The ITV contains pressure-sensitive valves and is designed to selectively impede the gas influx through the airway during chest-wall decompression. During chest decompression, pressure in the upper airways decreases, inducing the closure of the valve and preventing the gases from entering the lungs. Coupled with ACD, the ITV will thereby augment the amplitude and the duration of the vacuum within the thorax during active decompression [28], enhancing venous return and cardiac preload. The increase in cardiac filling during decompression will result in an increase in cardiac output during the next compression. The cracking pressure, defined as the inspiratory pressure needed to allow gases to flow inwards through the valve, usually varies from -7 to -16 cmH2O. Current evidence supports the use of ITV with a cracking pressure of -7 cmH2O for standard CPR and -15 cmH2O for ACD CPR.
 

(Crit Care Med 2007;35:1145)
experimental study on impedance threshold device to improve BP in central hypovolemia

Post-Resus

Avoid hyperthermia for all patients after resuscitation. Consider inducing hypothermia if the patient is unresponsive, but with an adequate blood pressure following resuscitation.
 

Unconscious adult patients with ROSC after out-of-hospital cardiac arrest should be cooled to 32ºC to 34°C for 12 to 24 hours when the initial rhythm was VF (Class IIa). Similar therapy may be beneficial for patients with non-VF arrest out of hospital or for in-hospital arrest (Class IIb).

Complete guidelines: AHA Download Site.

Bradycardia

Algorithm is now divided into well-perfused patients and inadequately perfused patients.
For the stable group, we do nothing.
 

For the unstable patients, try the following:

• Prepare for transcutaneous pacing without delay for high-degree block.
• Give Atropine
  Atropine Dosing is new; it is now 0.5 mg IV (not 0.5-1 mg). The atropine may be repeated to a total dose of 3 mg. Can try in high degree blocks while awaiting a pacer.
• Isuprel is gone! If you need to move up on the drug chain, use epi or dopamine.
   

 

 

Tachycardia

The goal of the ACLS gurus was to simplify therapy and distill the information in the algorithm to the essence of care required for initial stabilization and evaluation in the first hours of therapy (i.e. not some ridiculous protocol involving your knowledge of the patient's ejection fraction).

The algorithm divides patients into stable/unstable, wide/narrow, and regular/irregular.

Check out the algorithm here:



Notable changes are:

Polymorphic V-Tach
If a patient has polymorphic VT and is unstable, treat the rhythm as VF and deliver high-energy unsynchronized shocks (360J only).

Cardioversion
Shock Afib starting at 100 to 200
Other tachycardias may start 50 to 100
 

Poor Prognostic Signs

Bilateral absence of cortical response to median nerve somatosensory-evoked potentials measured 72 hours (in the normothermic patient) after hypoxic-ischemic (asphyxial) insult

• Absent corneal reflex at 24 hours

• Absent pupillary response at 24 hours

• Absent withdrawal response to pain at 24 hours

• No motor response at 24 hours

• No motor response at 72 hours

Stroke

tPA Improves Outcome When

Administered With Strict Criteria

2005 (New): Administration of IV tPA to

patients with acute ischemic stroke who

meet the National Institute of Neurologic

Disorders and Stroke (NINDS) eligibility

criteria is recommended if tPA is

administered by physicians in the setting of

a clearly defi ned protocol, a knowledgeable

team, and institutional commitment (Class

I). Note that the superior outcomes reported

in both community and tertiary-care

hospitals in the NINDS trials have been

diffi cult to replicate in hospitals with less

experience in, and institutional commitment

to, acute stroke care.

Is This Patient Dead, Vegetative, or Severely Neurologically Impaired?

(Jama Vol. 291 No. 7, February 18, 2004)

Physical Examination Maneuvers

In addition to the GCS, various brainstem reflexes are used in the physical examination of comatose patients.10, 12 The pupillary reflex involves cranial nerves II and III. Shining a penlight into one eye and then the other tests the patient's pupillary light response; the examiner observes the direct and consensual response (constriction of the opposite eye). The corneal reflex involves cranial nerves V and VII. Touching the cornea with a piece of cotton or tissue should cause both eyes to blink. The gag and cough reflexes test cranial nerves IX and X. To elicit a gag, apply a tongue depressor to the posterior pharynx. The soft palate should rise symmetrically. In patients who are intubated, assess the cough (or carinal) reflex by applying deep suction through the endotracheal tube to the carina. The suction will produce a gasp followed by several rapid coughs.

Vestibular signs are also commonly examined in the comatose patient. The oculocephalic (or "Doll's eye") reflex involves observing the patient's eyes during passive rotation of the skull. In a comatose patient with intact midbrain and vestibular reflexes, the eyes will move in a direction opposite to that in which the head is moved. If this reflex is lost, the globes will remain fixed within the head and the eyes will continue to stare in whatever direction the head is pointed. This reflex should not be tested in cases of suspected cervical trauma. Cold water caloric testing (oculovestibular reflex) also tests the vestibular and oculomotor systems. To perform the test, first examine the tympanic membrane to ensure there is no perforation or impacted cerumen. With the head 30° higher than the horizontal, irrigate up to 120 mL of ice cold water into the auditory canal. In the unconscious patient with intact brainstem function, there will be slow tonic deviation of eyes towards the irrigated ear.

It is also important to note the presence of seizures or myoclonus when examining the comatose patient, for some clinicians believe they may be useful in prognosis of comatose survivors of cardiac arrest. Seizures may be generalized or focal. Myoclonus refers to isolated sudden muscular contractions and may be either focal or generalized contractions of axial and limb musculature. In patients with seizures, the physical examination should be repeated after the postictal period.

Finally, mechanically ventilated patients are frequently sedated and/or paralyzed. Accordingly, when performing a detailed neurological examination it is crucial that these medications be at least temporarily discontinued.

Summary

Summary measures for clinical variables that were assessed in at least 3 studies are presented in Table 5. Five pooled variables were found to have a 95% CI lying entirely above 1. The clinical signs at 24 hours with the highest LRs were absent corneal reflexes (LR, 12.9; 95% CI, 2.0-68.7), absent pupillary reflexes (LR, 10.2; 95% CI, 1.8-48.6), absent motor response (LR, 4.9; 95% CI, 1.6-13.0), and absent withdrawal to pain (LR, 4.7; 95% CI, 2.2-9.8). At 72 hours after cardiac arrest, absent motor response was found to accurately predict death or poor neurological outcome (LR, 9.2; 95% CI, 2.1-49.4). No clinical findings were found to accurately predict good neurological outcome (ie, no useful negative LRs).

Rescuers hyperventilate patients and this leads to poorer outcomes (CCM Volume 32(9) September 2004) 

Thrombolytics

Thrombolysis for MI. Gave all patients without pulse TNKase. 36 ABI in ROSC (Resus 2004;61:309-313)

Review (Emerg Med J 2006;23:747)

MIs need cath after cardiac arrest

8 P. Garot, T. Lefevre and H. Eltchaninoff et al., Six-month outcome of emergency percutaneous coronary intervention in resuscitated patients after cardiac arrest complicating ST-elevation myocardial infarction, Circulation 115 (2007), pp. 1354–1362. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (0)

9 V. Gorjup, P. Radsel, S.T. Kocjancic, D. Erzen and M. Noc, Acute ST-elevation myocardial infarction after successful cardiopulmonary resuscitation, Resuscitation 72 (2007), pp. 379–385. SummaryPlus | Full Text + Links | PDF (109 K) | View Record in Scopus | Cited By in Scopus (2)

How to best Perform CPR

ACLS does not improve out of hospital survival, cpr and rapid shock are far more important (NEJM 2004;351(7):647-656) by Ian G. Stiell

best cpr is probably just rapid chest compressions with a inspiratory impedance valve preventing ventilation during decompression.

Ventilations not so important; eliminate from community cpr

Ventilation may actually be detrimental (Curr Opin Crit Care 2005;11:212)

Mechanical Devices

impedance threshold device-

An impedence threshold device (ITD) is a device added into the respiratory circuit (between the endotracheal tube or mask and bag-valve) to impede the influx of respiratory gases into the chest during the chest wall recoil phase of cardiopulmonary resuscitation (CPR).

Adverse effects of positive pressure ventilation include an increase in intrathoracic pressure, and the inability to develop a negative intrathoracic pressure during the release phase of chest compression. Positive pressure ventilation inhibits venous return to the thorax and right heart and thus results in decreased coronary and cerebral pressures. Another aspect of hyperventilation and increased intrathoracic pressure is its adverse effect on intracranial pressure and cerebral perfusion pressure [22,23]. These adverse effects are compounded by the fact that ventilation rates by physicians as well as paramedic rescuers are often much faster than the rate recommended by the guidelines, and unfortunately are still significantly above those recommended even after extensive retraining [20,21]. During cardiac arrest, faster ventilation rates increase the mean intra thoracic pressure and further impede forward blood flow.
 

predictors of outcome in cardiopulmonary resuscitation: systematic review (Emerg. Med. J. 2005;22;700-705)

We have no idea what people really die of in the ED (Emerg. Med. J. 2005;22;718-721)

Chest Compression in first 5 minutes of code with and without ventilations; no change in outcomes. NEJM 2000;342(21):1546

Chest compression efficacy not reflected by pulse, ETCO2 is the way to tell (

 Open Chest massage is better ([Benson
DM, O'Neil BO, Kakish E, Erpelding J, et al: Open chest CPR improves
survival and neurologic outcome following cardiac arrest. RESUSCITATION
2005; 64: 209-217.])

review of lytics in arrest (Minerva anestesiol 2005;71:291)

Survival for in-hopsital arrest in adults is ~18% (JAMA 2006;295 50-57)

Cerebroprotective resuscitation

Mike Darwin Article

Calcium Channel Blockers

Free Radical Blockers: Vitamin E, Selenium, Vitamin C, b-carotene

Quinacrine

Acetyl-l-carnitine

Haemodynamics of Arrest

Curr Opin Crit Care 2006;12:198

CPP=Ao-RA

Coronary perfusion pressure is the most important determinant for successful defib

takes up 12 beats to build up aortic pressure

Time sensitive Model of Arrest

JAMA 2002;288(23):3035

3 phase model

Electrical Phase 0-4 minutes

easy to shock out

Circulatory Phase 4-10 minutes

need compressions before shock

Metabolic Phase >10 minutes

hypothermia attenuates injury

Predicting Outcome

(Neurology 2006;67:203)

Percussion Pacing

Suspended animation

suspended animation article (Crit Care Med 1996;24(2S):24S)
 

History of Resuscitation

history of resuscitation (Crit Care Med 1996;24(Supp):S3)

Compression rate is obviously suboptimal in the hospital (Circulation 2005;111(4):428)

End Tidal CO2

Can cardiac sonography and capnography be used independently and in combination to predict resuscitation outcomes?

OBJECTIVE: To measure the ability of cardiac sonography and capnography to predict survival of cardiac arrest patients in the emergency department (ED). METHODS: Nonconsecutive cardiac arrest patients prospectively underwent either cardiac ultrasonography alone or in conjunction with capnography during cardiopulmonary resuscitation at two community hospital EDs with emergency medicine residency programs. Cardiac ultrasonography was carried out using the subxiphoid view during pauses for central pulse evaluation and end-tidal carbon dioxide (ETCO(2)) levels were monitored by a mainstream capnograph. A post-resuscitation data collection form was completed by each of the participating clinicians in order to assess their impressions of the facility of performance and benefit of cardiac sonography during nontraumatic cardiac resuscitation. RESULTS: One hundred two patients were enrolled over a 12-month period. All patients underwent cardiac sonographic evaluation, ranging from one to five scans, during the cardiac resuscitation. Fifty-three patients also had capnography measurements recorded. The presence of sonographically identified cardiac activity at any point during the resuscitation was associated with survival to hospital admission, 11/41 or 27%, in contrast to those without cardiac activity, 2/61 or 3% (p < 0.001). Higher median ETCO(2) levels, 35 torr, were associated with improved chances of survival than the median ETCO(2) levels for nonsurvivors, 13.7 torr (p < 0.01). The multivariate logistic regression model, which evaluated the combination of cardiac ultrasonography and capnography, was able to correctly classify 92.4% of the subjects; however, of the two diagnostic tests, only capnography was a significant predictor of survival. The stepwise logistic regression model, summarized by the area under the receiver operator curve of 0.9, furthermore demonstrated that capnography is an outstanding predictor of survival. CONCLUSIONS: Both the sonographic detection of cardiac activity and ETCO(2) levels higher than 16 torr were significantly associated with survival from ED resuscitation; however, logistic regression analysis demonstrated that prediction of survival using capnography was not enhanced by the addition of cardiac sonography.(Acad Emerg Med. 2001 Jun;8(6):610-5.)

Late values (20 minutes from onset of ACLS) of <10 = no survival (NEJM 1997;337:301)