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The answer is simple.

If the patient is acidotic, then the bicarb will improve the pH in the short

term which may help correct and stabilize the cardiac electrical system

Don't give it unless you are properly ventilating the patient!

If the patient is hyperkalemic to start off with, as in the cause of arrest....

then bicarb won't help. If working a dialysis code, after infusing large amounts

of fluid and starting with epi and atropine/lidocaine, then giving calcium, then

try some bicarb. It wont hurt to try albuterol as well, but it really isnt a

code drug.... fact is, they all take time, more time then we are going to give

most codes.

If the patient has arrested for some cause other then acidocis or hypoxia, it is

doubtful that by the time you get to bicarb you will saving anything.

Save your bicarb for post-arrest resuscitations, TCA OD's, respiratory arrests

leading to cardiac arrests, where it is more likely to be of benefit.

;-)

Nick

____________________________________________

Nick Nudell, NREMT-P, CCEMT-P

California

nudell@...

" Perception is reality " - Wise Old Paramedic

bicarb

Ok here is a question for the group. I had the chance to ask this of three

cardiologist and got three differnt answers and caused a very intense

discussion amungst them.

In a cardiac arrest situation, would the use of sodium bicarbonate be an

advantage?

I do not know the answer to this. Nor of any study on the subject. This

is simply a question and maybe even something to think about.

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Nick:

I am not sure where you get your medical facts, but may want to re-check

them before posting to a list.

1. There are some codes where bicarb will help, although most simply require

ventilation.

2. Dialysis patients with hyperkalemia need calcium (calcium gluconate,

calcium chloride). All the other drugs are useless unless you lower the

potassium.

3. How many people have cardiac arrests secondary to " acidosis " (except in

patient restraint with excited delirium)? The remainder of which have

acidosis secondary to other causes.

Re: bicarb

The answer is simple.

If the patient is acidotic, then the bicarb will improve the pH in the short

term which may help correct and stabilize the cardiac electrical system

Don't give it unless you are properly ventilating the patient!

If the patient is hyperkalemic to start off with, as in the cause of

arrest.... then bicarb won't help. If working a dialysis code, after

infusing large amounts of fluid and starting with epi and

atropine/lidocaine, then giving calcium, then try some bicarb. It wont hurt

to try albuterol as well, but it really isnt a code drug.... fact is, they

all take time, more time then we are going to give most codes.

If the patient has arrested for some cause other then acidocis or hypoxia,

it is doubtful that by the time you get to bicarb you will saving anything.

Save your bicarb for post-arrest resuscitations, TCA OD's, respiratory

arrests leading to cardiac arrests, where it is more likely to be of

benefit.

;-)

Nick

____________________________________________

Nick Nudell, NREMT-P, CCEMT-P

California

nudell@...

" Perception is reality " - Wise Old Paramedic

bicarb

Ok here is a question for the group. I had the chance to ask this of three

cardiologist and got three differnt answers and caused a very intense

discussion amungst them.

In a cardiac arrest situation, would the use of sodium bicarbonate be

an

advantage?

I do not know the answer to this. Nor of any study on the subject.

This

is simply a question and maybe even something to think about.

Link to comment
Share on other sites

After reading what you wrote, I thought we were saying the same thing.

Thanks...

Nick

bicarb

Ok here is a question for the group. I had the chance to ask this of three

cardiologist and got three differnt answers and caused a very intense

discussion amungst them.

In a cardiac arrest situation, would the use of sodium bicarbonate be

an

advantage?

I do not know the answer to this. Nor of any study on the subject.

This

is simply a question and maybe even something to think about.

Link to comment
Share on other sites

I did some research this afternoon while the doorbell was ringing.... I

looked back on Medline for 30 years regarding hyperkalemia and about 8 years for

bicarb. I did not look at the titles related to arrests from blood transfusions,

surgeries or other etiologies not pertinent to this discussion. I also ignored

some but not all animal studies. I found some interesting reading and am sharing

some of those abstracts with you here.

AHA lists both calcium and bicarb as class Indeterminate drugs. This is

because no study has shown that either medication will benefit a significant

number of patients. This does not mean that some people will not benefit from

them (for example, hyperK patients). I have included a couple abstracts that are

related to some of the recent research on delayed defibrillation that show some

promising results. The studies are geared towards neurologic function

post-resuscitation but are postive nonetheless.

In every single case, except for one that did not provide adequate info to

determine if its true or not, the published cases of hyperkalemic patients who

have been resuscitated... were resuscitated after long periods of CPR (like

90-120 minutes) and standard ACLS as well as 'standard' treatments for hyperK,

which where then followed by hemodialysis leading to SROSC (Spontaneous return

of circulation). These cases were not in the context of my previous message but

are discussed when I am teaching ACLS to nurses and doctors who 'may' be able to

initiate dialysis.

So finally, my comments were within the context of the current AHA

guidelines. Similar comments would have applied had anyone asked about epi or

lidocaine or atropine... all have minimal impact on the greater number of

arrests, while some patients will benefit from them.

Basically, what every survivable arrest patient benefits from and is

something we can do- circulation and ventilation. Although I have provided one

or two abstracts here that would seemingly disprove that theory also.

If anyone disagrees with what I have posted, please feel free to comment

or discuss! That is why I am here, to learn from y'all! (in my best Texas

accent)

Have a great weekend!

Nick

______________________________________

Resuscitation. 1996 Jul;32(1):27-9.

Unexpected return of cardiac action after termination of cardiopulmonary

resuscitation.

Voelckel W, Kroesen G.

Department of Anaesthesia and Intensive Care Medicine,

Leopold-Franzens-University of Innsbruck, Austria.

Application of sodium bicarbonate is still an option when resuscitation efforts

remain unsuccessful. Despite this, there are no recommendations on how long

resuscitation should be performed after administration of this drug. Here we

describe a case in which prehospital resuscitation efforts were terminated about

35 min after cardiac arrest. Seven minutes after all efforts had been

discontinued, spontaneous sinus rhythm appeared from a zero-line ECG, giving

normal hemodynamic values. The underlying reason might be unexpected and

unrecognized hyperkalemia, which was diminished by administration of sodium

bicarbonate, even under the conditions of cardiocirculatory arrest.

--------------------------------------------------------------------------------\

---------------------------

Ann Emerg Med. 1994 Aug;24(2):305-11.

Prolonged asystolic hyperkalemic cardiac arrest with no neurologic sequelae.

Quick G, Bastani B.

Division of Emergency Medicine, St Louis University Medical Center, Missouri.

We report the case of a 70-year-old man who developed cardiac arrest secondary

to hyperkalemia that complicated severe chronic renal failure due to obstructive

uropathy. The patient experienced electromechanical dissociation and

approximately 26 minutes of asystole after which the resuscitation was

suspended. However, 8 to 10 minutes after declaration of death, the patient was

noted to have developed spontaneous return of circulation as the emergency

department personnel were preparing to transport him to the morgue. The patient

survived and was discharged without apparent neurologic sequelae. This case

demonstrates the challenges facing physicians to predict the outcome of

hyperkalemic cardiac arrest based on usual parameters. It also highlights the

relative paucity of resuscitation guidelines to assist in the management of this

medical emergency.

--------------------------------------------------------------------------------\

-------------

Intensive Care Med. 1994;20(4):287-90.

Outcomes of severe hyperkalemia in cardiopulmonary resuscitation with

concomitant hemodialysis.

Lin JL, Lim PS, Leu ML, Huang CC.

Division of Nephrology, Chang Gung Memorial Hospital, Taipei, Taiwan, R.O.C.

OBJECTIVE: To investigate the efficacy of hemodialysis during cardiopulmonary

resuscitation as an effective adjunct to the treatment of severe hyperkalemia.

DESIGN: A prospective study. SETTING: In hospital dialysis units and intensive

care units. PATIENTS: Renal failure patients who developed hyperkalemia induced

cardiac arrest and failed to recover from conventional cardiopulmonary

resuscitation (CPR) were included. Three patients entered into this study: 2

patients with chronic renal failure maintained on regular hemodialysis and one

with acute renal failure who suffered from severe hyperkalemia. INTERVENTIONS:

All three patients developed asystolic cardiac arrest with unrecordable blood

pressure due to severe hyperkalemia. Aggressive CPR together with intravenous

epinephrine, sodium bicarbonate and calcium chloride were instituted. External

cardiac massage with cardiac defibrillation was unable to restore spontaneous

heart action. After lack or response to intensive resuscitation, hemodialysis

was performed concomitant with CPR to eliminate the potassium load. MEASUREMENTS

AND RESULTS: Sinus rhythm and blood pressure were restored in all 3 patients but

one of them eventually succumbed to her underlying disease. CONCLUSION:

Hemodialysis during CPR is probably an effective adjunct to the treatment of

severe hyperkalemia in patients with severe hemodynamic compromise and asystolic

cardiac arrest.

--------------------------------------------------------------------------------\

-

Heart Lung. 1993 Nov-Dec;22(6):548-53.

Changes in the pharmacotherapy of CPR.

Grillo JA, ER.

School of Pharmacy, Virginia Commonwealth University, Medical College of

Virginia.

The objective of this study was to review current changes in the pharmacologic

management of cardiac arrest (ventricular fibrillation, pulseless ventricular

tachycardia, asystole, and electromechanical dissociation) as put fourth by the

American Heart Association's 1992 Guidelines for Cardiopulmonary Resuscitation

and Emergency Cardiac Care. We concluded that the 1992 Guidelines provide a

reference base for all clinicians involved in emergency cardiac care. The newly

revised recommendations are classified on the basis of the true clinical merit

of the intervention, for example, an intervention that has been proved effective

(i.e., high-dose epinephrine) versus one that is possibly effective (i.e.,

high-dose epinephrine). The preferred intravenous fluid to be used in

resuscitation is saline solution or lactated ringers solution because of

possible adverse neurologic outcomes seen with dextrose-containing fluids. The

dose of all drugs administered via the endotracheal route should be 2 to 2.5

times the intravenous dose. Modifications in the dose or dosing interval have

been recommended for epinephrine, atropine, lidocaine, bretylium, and

procainamide during cardiopulmonary resuscitation. Options for high-dose

epinephrine therapy are offered, but neither recommended or discouraged.

Magnesium sulfate has been added for the management of torsades de points,

severe hypomagnesemia, or refractory ventricular fibrillation. The maximum total

dose of atropine in the treatment of asystole and electromechanical dissociation

has been increased from 2 mg to 0.04 mg/kg. The use of sodium bicarbonate should

be limited to the treatment of hyperkalemia, tricyclic antidepressant overdose,

overdoses requiring urinary alkalinization, or preexisting bicarbonate sensitive

acidosis.

--------------------------------------------------------------------------------\

--

Wis Med J. 1990 Aug;89(8):459-61.

Hyperkalemic electromechanical dissociation.

Lawton JM.

St 's Regional Kidney Dialysis Program, Green Bay, WI.

Two patients with hyperkalemic electromechanical dissociation are described.

Electrocardiograms at the time of the cardiac arrests demonstrated normal

appearing QRS complexes. Both patients responded to intravenous calcium chloride

administration with prompt restoration of normal blood pressure. Implications of

these observations with respect to current advanced cardiac life support

guidelines are discussed.

--------------------------------------------------------------------------------\

---------------------------

Ann Fr Anesth Reanim. 1990;9(3):204-7.

[Pharmacology of cardiopulmonary resuscitation]

[Article in French]

Hoffmann AC, Scheidegger D.

Departement d'Anesthesie, Hopital Cantonal Universitaire, Bale.

Among the adrenergic receptor agonists, epinephrine, at alpha and beta

stimulating doses, remains the drug of choice for cardiopulmonary resuscitation.

However, alpha adrenergic agonists such as phenylephrine, methoxamine and

dopamine (at alpha stimulating doses) result in similar success rates of

resuscitation as epinephrine. In the opposite, beta adrenergic agonists, without

or with only low alpha stimulating effect, such as isoproterenol or dobutamine

are significantly less efficient. There are few data indicating that sodium

bicarbonate improves outcome. Moreover it carries the risk of adverse effects.

It may be of benefit in case of preexisting metabolic acidosis or during

prolonged resuscitation with documented acidosis. Calcium remains indicated in

case of hypocalcaemia, hyperkalaemia or calcium channel blocker intoxication.

Severe ionized hypocalcaemia can occur after out-of-hospital cardiac arrest

--------------------------------------------------------------------------------\

------------------------------

J Emerg Med. 1989 Mar-Apr;7(2):109-13.

Hyperkalemia during human cardiopulmonary resuscitation: incidence and

ramifications.

GB, Nowak RM, Cisek JE, Carden DL, Tomlanovich MC.

Department of Emergency Medicine, Henry Ford Hospital, Detroit, MI 48202.

Although hypokalemia has been reported after cardiac arrest and successful

resuscitation, experimental data indicate that potassium is released from cells

during ischemia. The purpose of this investigation was to study serum potassium

concentration ([K+]) during closed chest cardiopulmonary resuscitation (CC-CPR)

in humans. Twenty-two patients presenting to the emergency department (ED) in

cardiopulmonary arrest had simultaneous measurement of central venous and

arterial [K+] and blood gases during CC-CPR utilizing current advanced cardiac

life support protocols and a pneumatic chest compressor and ventilator. Mean

arterial and central venous [K+] were 5.0 +/- 1.3 and 5.6 +/- 2.9 mEq/L,

respectively, (p greater than .05) with 7 patients having [K+] of greater than 6

mEq/L. Significant hyperkalemia does occur in some patients during cardiac

arrest and CC-CPR. Because poor tissue perfusion during CC-CPR impairs exchange

between the interstitial and intravascular compartments, increases in

interstitial [K+] would be expected to be even greater. Interstitial

hyperkalemia may play a role in the genesis of wide complex electromechanical

dissociation (EMD) seen after prolonged cardiac arrest. Since calcium has long

been known to be beneficial in the treatment of hyperkalemia-induced

dysrhythmias, the success of calcium chloride in treating wide complex EMD may

be on the basis of this phenomenon.

--------------------------------------------------------------------------------\

------------------------------------

Intensive Care Med. 1989;15(5):325-6.

Hyperkalemic cardiac arrest, prolonged heart massage and simultaneous

hemodialysis.

Torrecilla C, de la Serna JL.

Intensive Care Unit, Clinica Puerta de Hierro, Madrid, Spain.

A 53 year old diabetic patient underwent CABG and aortic valve replacement in

another institution and developed postoperative oliguric and hyperkalemic acute

renal failure. Shortly after transferring to our unit a cardiac arrest occurred.

Immediate resuscitative measures were ineffective. The serum potassium level was

10.2 mmol/l. Conventional arteriovenous hemodialysis was initiated while the

patient was still undergoing cardiac massage. When the serum potassium level was

lowered to 6.5 mmol/l, 90 min later, the heart began to beat. After hemodialysis

was discontinued the patient was reactive and fully conscious. The use of

simultaneous hemodialysis with prolonged mechanical heart massage as a reliable

method for recovery in hyperkalemic cardiac standstill is stressed.

--------------------------------------------------------------------------------

Am J Kidney Dis. 1985 Jan;5(1):47-8. Related Articles, Links

Lethal hyperkalemia associated with severe hyperglycemia in diabetic patients

with renal failure.

Montoliu J, Revert L.

Two patients with diabetic nephropathy on maintenance hemodialysis developed

extreme hyperkalemia (7.9 and 9.3 mmol/L, respectively) in association with

severe episodes of hyperglycemia (1,152 and 1,185 mg/dL, respectively). The

increase in serum potassium was out of proportion to the degree of metabolic

acidosis that both patients had, and no exogenous source of hyperkalemia could

be identified. Despite treatment efforts both patients died shortly after

arrival as a consequence of cardiac arrest. It is proposed that the

hyperosmolality of extracellular fluid produced by severe hyperglycemia drives

potassium passively out of the cells, therefore favoring the rapid development

of hyperkalemia. Insulin deficiency could also play a role. This situation is

particularly dangerous in individuals with impaired renal function. Adequate

blood glucose control in diabetic patients on dialysis is important to avoid

life-threatening hyperkalemia.

---------------------------------------------------------------------------

Anaesthesist. 1983 Sep;32(9):443-4.

[Asystole in extreme hyperkalemia, and successful resuscitation]

[Article in German]

Kretz FJ, Meschede V.

Cardiac arrest in a twenty-year-old patient was caused by hyperkalaemia of 11.8

mmol/l. Cardiorespiratory resuscitation and emergency treatment of hyperkalaemia

saved the life of this patient without residual neurological or mental

disorders. We discuss pathophysiological mechanisms.

-------------------------------------------------------------------------------

Resuscitation. 2001 Dec;51(3):309-15.

Sodium bicarbonate improves the chance of resuscitation after 10 minutes of

cardiac arrest in dogs.

Leong EC, Bendall JC, Boyd AC, Einstein R.

Department of Pharmacology, University of Sydney, NSW 2006, Sydney, Australia.

The likelihood of successful defibrillation and resuscitation decreases as the

duration of cardiac arrest increases. Prolonged cardiac arrest is also

associated with the development of acidosis. These experiments were designed to

determine whether administration of sodium bicarbonate and/or adrenaline in

combination with a brief period of cardiopulmonary resuscitation (CPR) prior to

defibrillation would improve the outcome of prolonged cardiac arrest in dogs.

Ventricular fibrillation (VF) was induced by a.c. shock in anaesthetised dogs.

After 10 min of VF, animals received either immediate defibrillation (followed

by treatment with bicarbonate or control) or immediate treatment with

bicarbonate or saline (followed by defibrillation). Treatment with bicarbonate

was associated with increased rates of restoration of spontaneous circulation.

This was achieved with fewer shocks and in a shorter time. Coronary perfusion

pressure was significantly higher in NaHCO3-treated animals than in control

animals. There were smaller decreases in venous pH in NaHCO3-treated animals

than in controls. The best outcome in this study was achieved when

defibrillation was delayed for approximately 2 min, during which time NaHCO3 and

adrenaline were administered with CPR. The results of the present study indicate

that in prolonged arrests bicarbonate therapy and a period of perfusion prior to

defibrillation may increase survival.

------------------------------------------------------------------------------

Resuscitation. 2002 Oct;55(1):45-55.

Buffer administration during CPR promotes cerebral reperfusion after return of

spontaneous circulation and mitigates post-resuscitation cerebral acidosis.

Liu X, Nozari A, Rubertsson S, Wiklund L.

Uppsala University Hospital, Department of Surgical Sciences/Anesthesiology and

Intensive Care, SE-751 85 Uppsala, Sweden.

To explore the effects of alkaline buffers on cerebral perfusion and cerebral

acidosis during and after cardiopulmonary resuscitation (CPR), 45 anaesthetized

piglets were studied. The animals were subjected to 5 min non-interventional

circulatory arrest followed by 7 min closed chest CPR and received either 1

mmol/kg of sodium bicarbonate, 1 mmol/kg of tris buffer mixture, or the same

volume of saline (n=15 in all groups), adrenaline (epinephrine) boluses and

finally external defibrillatory shocks. Systemic haemodynamic variables,

cerebral cortical blood flow, arterial, mixed venous, and internal jugular bulb

blood acid-base status and blood gases as well as cerebral tissue pH and PCO(2)

were monitored. Cerebral tissue acidosis was recorded much earlier than arterial

acidaemia. After restoration of spontaneous circulation, during and after

temporary arterial hypotension, pH in internal jugular bulb blood and in

cerebral tissue as well as cerebral cortical blood flow was lower after saline

than in animals receiving alkaline buffer. Buffer administration during CPR

promoted cerebral cortical reperfusion and mitigated subsequent

post-resuscitation cerebral acidosis during lower blood pressure and flow in the

reperfusion phase. The arterial alkalosis often noticed during CPR after the

administration of alkaline buffers was caused by low systemic blood flow, which

also results in poor outcome.

--------------------------------------------------

Resuscitation. 2002 Jul;54(1):47-55.

Clinical use of sodium bicarbonate during cardiopulmonary resuscitation--is it

used sensibly?

Bar-ph G, Abramson NS, Jansen-Mc L, Kelsey SF, Mashiach T, Craig MT,

Safar P; Brain Resuscitation Clinical Trial III (BRCT III) Study Group.

Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh,

PA 15260, USA. g_barjoseph@...

This study retrospectively analyzed the pattern of sodium bicarbonate (SB) use

during cardiopulmonary resuscitation (CPR) in the Brain Resuscitation Clinical

Trial III (BRCT III). BRCT III was a prospective clinical trial, which compared

high-dose to standard-dose epinephrine during CPR. SB use was left optional in

the study protocol. Records of 2915 patients were reviewed. Percentage, timing

and dosage of SB administration were correlated with demographic and cardiac

arrest variables and with times from collapse to Basic Life Support, to Advanced

Cardiac Life Support (ACLS) and to the major interventions performed during CPR.

SB was administered in 54.5% of the resuscitations. The rate of SB use decreased

with increasing patient age-primarily reflecting shorter CPR attempts. Mean time

intervals from arrest, from start of ACLS and from first epinephrine to

administration of the first SB were 29+/-16, 19+/-13, and 10.8+/-11.1 min,

respectively. No correlation was found between the rate of SB use and the

pre-ACLS hypoxia times. On the other hand, a direct linear correlation was found

between the rate of SB use and the duration of ACLS. We conclude that when SB

was used, the time from initiation of ACLS to administration of its first dose

was long and severe metabolic acidosis probably already existed at this point.

Therefore, if SB is used, earlier administration may be considered. Contrary to

physiological rationale, clinical decisions regarding SB use did not seem to

take into consideration the duration of pre-ACLS hypoxia times. We suggest that

guidelines for SB use during CPR should emphasize the importance of pre-ACLS

hypoxia time in contributing to metabolic acidosis and should be more specific

in defining the duration of " protracted CPR or long resuscitative efforts " , the

most frequent indication for SB administration

--------------------------------------------------

Acad Emerg Med. 1995 Apr;2(4):264-73.

Association of drug therapy with survival in cardiac arrest: limited role of

advanced cardiac life support drugs.

Stiell IG, Wells GA, Hebert PC, Laupacis A, Weitzman BN.

University of Ottawa Faculty of Medicine, Ontario, Canada.

OBJECTIVE: To generate hypotheses regarding the association of standard Advanced

Cardiac Life Support (ACLS) drugs with human cardiac arrest survival. METHODS:

This observational cohort study was conducted over a two-year period in the

wards, intensive care units, and EDs of two tertiary care hospitals. Included

werc adult patients who suffered cardiac arrest either inside or outside the

hospital and who required epinephrine according to standard ACLS guidelines. Six

standard ACLS drugs (given while CPR was in progress) were assessed for

association with survival from resuscitation to one hour and to hospital

discharge by univariate and multivariate logistic regression analyses. RESULTS:

In the 529 patients studied, initial cardiac rhythm had no impact on the

association between drug administration and survival. The time of drug

administration (quartile of ACLS period) was associated with resuscitation for

atropine (p < 0.05) and lidocaine (p < 0.01). The odds ratios (95% CIs) for

successful resuscitation, after multivariate adjustment for potential

confounders, were: a respiratory initiating cause, 3.7 (2.1 -6.4); each 5-minute

increase in CPR-ACLS interval, 0.5 (0.4-0.7); each 5-minute duration of ACLS.

0.9 (()1.8- 1.0; atropine, 1.2 (1.0-1.3); bretylium. (0.4 (0.1-1.1); calcium 0.8

(0.2-2.4); lidocaine, 0.9 (0.7-1.1); procainamide. 21.0 (5.2-84.0) d sodium

bicarbonate 1.2 (1.0-1.6). All other potential confounding variables entered

into the model were not significantly associated with resuscitation. CONCLUSION:

Initiating cause of arrest, time to ACLS, and duration of ACLS were important

correlates of survival. Other than procainaimide, standard ACLS drugs had

relatively little association with survival, but timing of administration may be

an important factor. Further research using definitive large randomized

controlled trials is warranted to assess the role of drug therapy in improving

cardiac arrest survival.

--------------------------------------------------------------

J Indian Med Assoc. 1999 Jul;97(7):259-64, 270.

Current concepts in cardiopulmonary resuscitation in adults.

Datta S, Nasr NF, Khorasani A, Datta R.

Department of Anaesthesiology and Pain Management, Cook County Hospital,

Chicago, USA.

Cardiopulmonary resuscitation (CPR) provides artificial circulation and

ventilation during cardiopulmonary arrest. CPR is further categorised as basic

life support (BLS), advanced cardiac life support (ACLS) and postresuscitation

support. BLS consists of provision of a patent upper airway, ventilation and

circulation of blood by closed chest cardiac compressions. ACLS includes use of

specialised equipment to maintain the airway, early defibrillation and

pharmacologic therapy. Successful outcome from an arrest depends on the total

duration of an arrest and early defibrillation, as ventricular fibrillation is

the most common cardiac rhythm found in adult cardiac arrest. Initial drug

therapy during CPR aims at correction of arterial hypoxaemia and restoring

coronary and cerebral perfusion. Oxygen and epinephrine constitute the mainstay

of drug therapy during CPR. In patients with ventricular tachycardia, lidocaine

is the drug of choice, followed by bretylium. Magnesium has proved to be useful

in both refractory pulseless ventricular tachycardia and fibrillation. Atropine

has not been demonstrated to improve outcome from arrest but can be administered

in bradyasystolic cardiac arrest. The routine administration of bicarbonate and

calcium is no longer recommended but situations exist where they can be used

appropriately. Administration of drugs during CPR should preferably be via a

central route, but epinephrine, lidocaine and atropine can be administered via

the endotracheal tube if intravenous access has not been established.

Postresuscitation care includes mechanical ventilation if necessary to optimise

oxygenation and ventilation and steps to maintain vital organ and optimal brain

protection, which includes avoidance of hypertension, hypotension and

hyperglycaemia.

____________________________________________

Nick Nudell, NREMT-P, CCEMT-P

California

nudell@...

" Perception is reality " - Wise Old Paramedic

RE: bicarb

Nick:

I am not sure where you get your medical facts, but may want to re-check

them before posting to a list.

1. There are some codes where bicarb will help, although most simply require

ventilation.

2. Dialysis patients with hyperkalemia need calcium (calcium gluconate,

calcium chloride). All the other drugs are useless unless you lower the

potassium.

3. How many people have cardiac arrests secondary to " acidosis " (except in

patient restraint with excited delirium)? The remainder of which have

acidosis secondary to other causes.

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Nick,

Have you found anything more recent? Granted, the studies seem to be very

relevant, but it looks as if it is against current practice to continue CPR

for any prolonged period of time. Is this a case of the medical community

forgetting the science, or is it that there have been more relevant studies

done? Or, am I way off base here? Thoughts?

Schadone, NREMT-Paramedic

City of Austin

Austin/ County EMS

Medic 12 / Medic 24

@...

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Mike

I provided all that I could find/access. Some of the recent literature (under a

couple years old) cannot be accessed in abstract or full-text files without

paying for it, like $30 each.

Keep in mind that termination of efforts should be considered when the case is

futile. Known cases of hypothermia, hyperkalemia, electrocution etc should not

be terminated until the conditions have been reversed, the conditions will not

reverse or the available equipment/training has been fully utilized. That is the

heart of the current recommendations.

Peoplecicles in Montana have been successfully resuscitated, even after being

pronounced twice in the field. This has not been published AFAIK. I do not have

firsthand knowledge of the events.

HyperK patients have spontaneously resuscitated even after 10 minutes after

termination of efforts. (no this is not a Halloween joke).

Pediatric primary cardiac arrest and electrocution are two cases that I can

think of off the top of my head where underlying CAD would not be a predominant

factor in the arrest and its possible that extended resuscitation might result

in neurologically and systemically intact survivors. No I have not specifically

done any recent lit searches on this... and cannot place my finger on where

exactly I learned these points.

Take care

Nick

____________________________________________

Nick Nudell, NREMT-P, CCEMT-P

California

nudell@...

" Perception is reality " - Wise Old Paramedic

RE: bicarb

Nick,

Have you found anything more recent? Granted, the studies seem to be very

relevant, but it looks as if it is against current practice to continue CPR

for any prolonged period of time. Is this a case of the medical community

forgetting the science, or is it that there have been more relevant studies

done? Or, am I way off base here? Thoughts?

Schadone, NREMT-Paramedic

City of Austin

Austin/ County EMS

Medic 12 / Medic 24

@...

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You know I really shoud have looked over my my question befor I sent it

out. Thats what I get for writting an email at 2 am I should have wrote the

use of bicarb early in the code vrs. later in the code in the case of renal

failure patients. When I was writting the question in my mind it sounded

what I ment it to say NOT what it realy did say. So after putting egg all

over my face I pose the correct question to the group , That will teach me

not to send emails out when I am tired/

One of the answers I did recieve was this. Renal failure patients have a

ph that acidotic on a normal bases. Normal for their condition that is. If a

RF pt, did suffer cadiac arrest the use of bicarb early vrs. late would

depend on how resent their last dialysis treatment was. One of the Md.s I

asked said that if the pt. had not hafd a treatment in two or more days that

indeed early bicarb maybe of an advantage. He also stated that there has not

been a study done to determine this question one way or the other. The

Doctors in questions or from St. Lukes and I asked them this when I was

transporting them to Hobby Airport. Now that the correct question has been

asked the post will make more sence to all who answered it.

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Ok, for your specific question... I did not find any studies that said after X

number of days since last dialysis you should use bicarb early.

I agree that renal failure patients are likely to be in an acidotic state, if

you find them arrested. This acidosis is a result of the hyperkalemic condition

caused by the renal failure. If you do not correct the hyperkalemia, then all

other treatments MAY be useless. In my previous post I had provided one case

example of a patient who had been treated for acidosis primarily, and was

resuscitated. I do not have access to the full case, so cannot be sure if

treatments for hyperkalemia were given as well.

So basically it will depend on your protocols.... you should start with your

'standard' ACLS meds (an exception possibly being a known dialysis patient),

because without having an I-Stat or some other electrolyte measuring device on

your ambulance, you cannot be certain if it is an electrolyte based arrest or a

cardiac arrest due to AMI or arrhythmia (so says AHA). If these standard

treatments do not work, then you would move on to other treatments, as per the

current ACLS guidelines and depending on your protocols. You can often detect

the hyperkalemia prior to arrest by a 12 lead EKG (I think I read about 20-25%

will have signs, which include tall symmetrical peaked T waves and an IVCD or

intraventricular conduction delay). The treatments for hyperkalemia include

bicarb (2 or more amps plus a drip which is D5 1L with 3 amps bicarb added),

insulin IVP(10u of regular), calcium (either gluconate or chloride which is

preferred in arrests but is better given through central lines), 25g glucose

(unless they are already hyperglycemic <like over 450-500>, then they will

possibly be unable to reabsorb the potassium as one paper I referenced

indicates), 25-50g of kayexelate (PO <via NG> or PR <via enema>), 10mg of

albuterol in continuous neb or IV (salbutamol)(will bring the K+ level down

about 0.5 which isn't much but will help). Then hemodialysis (might take 20-30

minutes of CPR during this to get an effect). Since insulin is not in most

ambulance drug packs, and is a prime med for hyperkalemia, will your protocols

allow you to administer a patients own insulin if found in a refrigerator in

their house or from a dialysis clinic perhaps??? Just remember that these meds

will take time to work, maybe something like half an hour, I have been told.

The current research, as I already mentioned, indicate that epi and bicarb might

be more beneficial in cardiac arrest patients if given prior to defibrillation,

and that 2 minutes is the most optimal time to defibrillate. This was not a

study specifically for hyperkalemia or dialysis. The bicarb in this case is

thought to reduce cerebral acidosis, which is believed to be a prime factor in

poor neurologic outcomes in the post-arrest patients.

I am not an expert on the subject but I have transported many renal failure

patients in the past leading me to become interested in the treatments they

specifically require. I am interested in whether the scope in Texas allows you

folks to be more aggressive with these patients then other states...?? Any

comments regarding this info?

Take care

Nick

____________________________________________

Nick Nudell, NREMT-P, CCEMT-P

California

nudell@...

" Perception is reality " - Wise Old Paramedic

Re: bicarb

You know I really shoud have looked over my my question befor I sent it

out. Thats what I get for writting an email at 2 am I should have wrote the

use of bicarb early in the code vrs. later in the code in the case of renal

failure patients. When I was writting the question in my mind it sounded

what I ment it to say NOT what it realy did say. So after putting egg all

over my face I pose the correct question to the group , That will teach me

not to send emails out when I am tired/

One of the answers I did recieve was this. Renal failure patients have a

ph that acidotic on a normal bases. Normal for their condition that is. If a

RF pt, did suffer cadiac arrest the use of bicarb early vrs. late would

depend on how resent their last dialysis treatment was. One of the Md.s I

asked said that if the pt. had not hafd a treatment in two or more days that

indeed early bicarb maybe of an advantage. He also stated that there has not

been a study done to determine this question one way or the other. The

Doctors in questions or from St. Lukes and I asked them this when I was

transporting them to Hobby Airport. Now that the correct question has been

asked the post will make more sence to all who answered it.

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