Jwade

Epocrates ABG Acid Plus Eponyms Netters Anatomy

Vasopressin Vasopressin is a nonadrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction.58,59 Despite 1 promising randomized study (LOE 2),60 additional lower-level studies (LOE 5),61–63 and multiple well-performed animal studies, 2 large randomized controlled human trials (LOE 1)64,65 failed to show an increase in rates of ROSC or survival when vasopressin (40 U, with the dose repeated in 1 study) was compared with epinephrine (1 mg, repeated) as the initial vasopressor for treatment of cardiac arrest. In the large multicenter trial involving 1186 out-of-hospital cardiac arrests with all rhythms (LOE 1),65 a post-hoc analysis of the subset of patients with asystole showed significant improvement in survival to hospital discharge but not neurologically intact survival when 40 U (repeated once if necessary) of vasopressin was used as the initial vasopressor compared with epinephrine (1 mg, repeated if necessary). A meta-analysis of 5 randomized trials (LOE 1)66 showed no statistically significant differences between vasopressin and epinephrine for ROSC, 24-hour survival, or survival to hospital discharge. The subgroup analysis based on initial cardiac rhythm did not show any statistically significant difference in survival to hospital discharge (LOE 1).66 In a large in-hospital study of cardiac arrest, 200 patients were randomly assigned to receive either 1 mg of epinephrine (initial rhythm: 16% VF, 3% VT, 54% PEA, 27% asystole) or 40 U of vasopressin (initial rhythm: 20% VF, 3% VT, 41% PEA, 34% asystole). There was no difference in survival to 1 hour (epinephrine: 35%, vasopressin: 39%) or to hospital discharge (epinephrine: 14%, vasopressin: 12%) between groups or subgroups.64 A retrospective analysis documented the effects of epinephrine alone (231 patients) compared with a combination of vasopressin and epinephrine (37 patients) in out-of-hospital cardiac arrest with VF/VT, PEA, or asystole. There was no difference in survival or ROSC when VF or PEA was the presenting rhythm, but ROSC was increased in the epinephrine plus vasopressin group among patients presenting with asystole.67 Because vasopressin effects have not been shown to differ from those of epinephrine in cardiac arrest, one dose of vasopressin 40 U IV/IO may replace either the first or second dose of epinephrine in the treatment of pulseless arrest (Class Indeterminate). 60. Lindner KH, Dirks B, Strohmenger HU, Prengel AW, Lindner IM, Lurie KG. Randomised comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation. Lancet. 1997; 349: 535–537.[CrossRef][Medline] [Order article via Infotrieve] 61. Lindner KH, Prengel AW, Brinkmann A, Strohmenger HU, Lindner IM, Lurie KG. Vasopressin administration in refractory cardiac arrest. Ann Intern Med. 1996; 124: 1061–1064.[Abstract/Free Full Text] 62. Mann K, Berg RA, Nadkarni V. Beneficial effects of vasopressin in prolonged pediatric cardiac arrest: a case series. Resuscitation. 2002; 52: 149–156.[CrossRef][Medline] [Order article via Infotrieve] 63. Morris DC, Dereczyk BE, Grzybowski M, Martin GB, Rivers EP, Wortsman J, Amico JA. Vasopressin can increase coronary perfusion pressure during human cardiopulmonary resuscitation. Acad Emerg Med. 1997; 4: 878–883.[Medline] [Order article via Infotrieve] 64. Stiell IG, Hebert PC, Wells GA, Vandemheen KL, Tang AS, Higginson LA, Dreyer JF, Clement C, Battram E, Watpool I, Mason S, Klassen T, Weitzman BN. Vasopressin versus epinephrine for inhospital cardiac arrest: a randomised controlled trial. Lancet. 2001; 358: 105–109.[CrossRef][Medline] [Order article via Infotrieve] 65. Wenzel V, Krismer AC, Arntz HR, Sitter H, Stadlbauer KH, Lindner KH. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med. 2004; 350: 105–113.[Abstract/Free Full Text] 66. Aung K, Htay T. Vasopressin for cardiac arrest: a systematic review and meta-analysis. Arch Intern Med. 2005; 165: 17–24.[Abstract/Free Full Text] 67. Guyette FX, Guimond GE, Hostler D, Callaway CW. Vasopressin administered with epinephrine is associated with a return of a pulse in out-of-hospital cardiac arrest. Resuscitation. 2004; 63: 277–282.[CrossRef][Medline] [Order article via Infotrieve]

ERDoc, I will try using the Sonosite the next time I drop a Femoral Line during a code to see if your premise is correct. It makes me wonder as well. One of my main thoughts on the subject is having worked as a First Assist in Trauma Surgery in Detroit, I have done countless IAM / IVM with contrast and I just have not seen all that much forward flow going on, even when we had an open chest and I was doing open cardiac massage with my hands and watching on the C-ARM. It would make for an interesting animal study i think. Dwayne, I think if you pull up the following study off Medline and read in entirety, it should help to clarify things for you about how Retrograde Anatomy and Flow can cause Femoral Pulsations. Connick M, Berg RA. Femoral venous pulsations during open-chest cardiac massage. Ann Emerg Med. 1994; 24: 1176–1179. Respectfully, JW

Cosgrojo, Points taken! So, let me try to simplify what I was asking. 1. Do you use Femoral Pulse checks to gauge CPR adequacy? 2. If " YES" please provide your rationale and literature. 3. If " NO" please explain your procedure and why. 4. What is your background and education. 5. Do you actually spend time reading and understanding current research literature? Again, Sorry for the confusion, I was not trying to flame anybody. I ask these questions because it is my experience having worked from the streets of Detroit to flying the friendly skies, when I ask a provider " WHY" he or she usually will say either, " that is what I was taught" or "that is the way we have always done it". Respectfully, JW

Et al... First, I was not trying to start a flame war by any means. However, I do not like people who state something as FACT and then cannot back it up with proven scientific evidence. I was always taught from DAY one in EMT BASIC school way back in 1992 that checking a femoral pulse was pointless. 1. Cardiac Output is 20% at best of normal 2. Finding Femoral Pulses in people is a difficult task many times even with Normal Cardiac Output. The reason I started this thread stemmed from a discussion / debate with an M.D. as I was teaching an ACLS course. A second reason I started the thread was having just finished an MBA program and having spent way too many hours looking at various HEMS / EMS statistics I was curious as to what the majority of responses would be, and from what background and education. (I.E. Street Paramedic, Flight Paramedic, EMT, Nurse, etc.....) I am more interested in the statistics. After pulling up the various studies which show femoral pulses during CPR = Retrograde Flow this physician has since changed his lectures to include this info to students. So, I am just curious as to what you guys do and WHY? Do you do it because that is what " we have always done" or " this is what i was taught" or do you alter your practice based on current literature? Also, I was not limiting the discussion to PRE-Hospital, I see many nurses checking femoral pulses in the ER during codes. I completely understand if you are limited in what you carry on the RIG due to medical direction and so forth. As a Flight Paramedic, we pretty much have every toy at our disposal, and waveform ETCo2 is used extensively in many different aspects of our patient care, especially when we are running on a vent. Anyways, I apologize if I offended anyone, it was not my intention. Also, Where did I make an assumption? I simply stated " ONE " must have a good working knowledge of A & P, I did NOT single any individual person out. Look forward to your continued responses. Respectfully, JW PS. MOBEY, What are you using for ETCo2? EasyCap or Waveform? There is a HUGE difference.

Herbie, First, Please don't regurgitate a bunch of anecdotal stories you have been taught your whole life. If one knew anything about anatomy and physiology one would understand that trying to feel a femoral pulse during the presence of CPR ( when cardiac output is at most 20% or normal) is nothing more than RETROGRADE BLOODFLOW! Again, one has to have a good understanding of what NORMAL anatomy is all about. For your reading pleasure. (Circulation. 2005;112:IV-78 – IV-83.) © 2005 American Heart Association, Inc. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care 8. Connick M, Berg RA. Femoral venous pulsations during open-chest cardiac massage. Ann Emerg Med. 1994; 24: 1176–1179. Assessment During CPR At present there are no reliable clinical criteria that clinicians can use to assess the efficacy of CPR. Although end-tidal CO2 serves as an indicator of cardiac output produced by chest compressions and may indicate return of spontaneous circulation (ROSC),1,2 there is little other technology available to provide real-time feedback on the effectiveness of CPR. Assessment of Hemodynamics Coronary Perfusion Pressure Coronary perfusion pressure (CPP = aortic relaxation [diastolic] pressure minus right atrial relaxation phase blood pressure) during CPR correlates with both myocardial blood flow and ROSC (LOE 3).3,4 A CPP of 15 mm Hg is predictive of ROSC. Increased CPP correlates with improved 24-hour survival rates in animal studies (LOE 6)5 and is associated with improved myocardial blood flow and ROSC in animal studies of epinephrine, vasopressin, and angiotensin II (LOE 6).5–7 When intra-arterial monitoring is in place during the resuscitative effort (eg, in an intensive care setting), the clinician should try to maximize arterial diastolic pressures to achieve an optimal CPP. Assuming a right atrial diastolic pressure of 10 mm Hg means that the aortic diastolic pressure should ideally be at least 30 mm Hg to maintain a CPP of 20 mm Hg during CPR. Unfortunately such monitoring is rarely available outside the intensive care environment. Pulses Clinicians frequently try to palpate arterial pulses during chest compressions to assess the effectiveness of compressions. No studies have shown the validity or clinical utility of checking pulses during ongoing CPR. Because there are no valves in the inferior vena cava, retrograde blood flow into the venous system produce femoral vein pulsations.8 Thus palpation of a pulse in the femoral triangle may indicate venous rather than arterial blood flow. Carotid pulsations during CPR do not indicate the efficacy of coronary blood flow or myocardial or cerebral perfusion during CPR. Assessment of Respiratory Gases Arterial Blood Gases Arterial blood gas monitoring during cardiac arrest is not a reliable indicator of the severity of tissue hypoxemia, hypercarbia (and therefore the adequacy of ventilation during CPR), or tissue acidosis. This conclusion is supported by 1 case series (LOE 5)9 and 10 case reports10–19 that showed that arterial blood gas values are an inaccurate indicator of the magnitude of tissue acidosis during cardiac arrest and CPR both in and out of hospital. Oximetry During cardiac arrest, pulse oximetry will not function because pulsatile blood flow is inadequate in peripheral tissue beds. But pulse oximetry is commonly used in emergency departments and critical care units for monitoring patients who are not in arrest because it provides a simple, continuous method of tracking oxyhemoglobin saturation. Normal pulse oximetry saturation, however, does not ensure adequate systemic oxygen delivery because it does not calculate the total oxygen content (O2 bound to hemoglobin + dissolved O2) and adequacy of blood flow (cardiac output). Tissue oxygen tension is not commonly evaluated during CPR, but it may provide a mechanism to assess tissue perfusion because transconjunctival oxygen tension falls rapidly with cardiac arrest and returns to baseline when spontaneous circulation is restored.20,21 End-Tidal CO2 Monitoring End-tidal CO2 monitoring is a safe and effective noninvasive indicator of cardiac output during CPR and may be an early indicator of ROSC in intubated patients. During cardiac arrest CO2 continues to be generated throughout the body. The major determinant of CO2 excretion is its rate of delivery from the peripheral production sites to the lungs. In the low-flow state during CPR, ventilation is relatively high compared with blood flow, so that the end-tidal CO2 concentration is low. If ventilation is reasonably constant, then changes in end-tidal CO2 concentration reflect changes in cardiac output. Eight case series have shown that patients who were successfully resuscitated from cardiac arrest had significantly higher end-tidal CO2 levels than patients who could not be resuscitated (LOE 5).2,22–28 Capnometry can also be used as an early indicator of ROSC (LOE 529,30; LOE 631). In case series totaling 744 intubated adults in cardiac arrest receiving CPR who had a maximum end-tidal CO2 of <10 mm Hg, the prognosis was poor even if CPR was optimized (LOE 5).1,2,24,25,32,33 But this prognostic indicator was unreliable immediately after starting CPR in 4 studies (LOE 5)1,2,32,33 that showed no difference in rates of ROSC and survival in those with an initial end-tidal CO2 of <10 mm Hg compared with higher end-tidal CO2. Five patients achieved ROSC (one survived to discharge) despite an initial end-tidal CO2 of <10 mm Hg. In summary, end-tidal CO2 monitoring during cardiac arrest can be useful as a noninvasive indicator of cardiac output generated during CPR (Class IIa). Further research is needed to define the capability of end-tidal CO2 monitoring to guide more aggressive interventions or a decision to abandon resuscitative efforts. In the patient with ROSC, continuous or intermittent monitoring of end-tidal CO2 provides assurance that the endotracheal tube is maintained in the trachea. End-tidal CO2 can guide ventilation, especially when correlated with the PaCO2 from an arterial blood gas measurement. Cheers. John Wade MBA, FP-C Kate, There is nothing wrong with being new and certainly not blonde. :-) It only means you have limited experience, and probably no critical care experience. Again, nothing wrong.. Your BLOOD PRESSURE is going to be the only reliable means of brain perfusion. Remember NORMAL CPP ( cerebral perfusion pressure is 70 for an adult. We can calculate CPP by taking your MAP - ICP = CPP Mean arterial pressure - Intercranial pressure = Cerebral Perfusion Pressure SO, For example, if you have someone with a ROSC, and a BP of 60 / 40. What is your CPP? Calculate MAP is Systolic + 2* Diastolic / 3 60+80 = 140 / 3 = MAP 46.6 Obviously we cannot calculate ICP without a bolt sticking out of the head, but a reliable estimate in a NON-Head Injured patient is 10% of your MAP. So a Map of 46 gives you 4.6 MAP - 46.6 ICP - 4.6 = CPP = 42 SO, we know that NORMAL adequate perfusion of CPP is 70, with the above BP you are at 42. It goes without saying, you are not doing a whole lot for his brain perfusion with a CPP of 42....... As far as ETC02 is concerned, THERE is a TON that WaveForm ETCo2 can tell someone. Again, this is far above your average 911 paramedic level training, but once you learn it and how to apply it in critical care settings, you will always want it......:-) Let me know if you have any questions. Respectfully, John Wade MBA, FP-C

Pain Relief in Arizona in the order I reach for it. Fentanyl Morphine and they keep getting it until they are pain free or not breathing. JW

In the age of practicing Evidence Based Medicine, I am curious how everyone guages if CPR is being performed effectively? I would also like you to document your answers with evidence and NOT anecdotal stories. For example, Do you check Femoral Pulse? Do you use EtCo2? Do you use an Art Line? Do you just make sure proper rate and depth are being performed? I will start the discussion with saying my practice is to use Proper Rate and Depth along with Waveform EtCo2. Femoral Pulse Checks are useless and should not be done. I have the studies to back this up, and will post them when we get some responses. Thanks in advance. JW

Hey Guys, I hope you are not stating categorically that MI patients need volume replacement? This would be seriously inaccurate. As far as NITRO dilating the coronary arteries, this has been proven false over and over again.....What NITRATES do cause are reduction of preload, which occurs due to dilatation of venous capacitance vessels, resulting in a decrease in myocardial oxygen consumption. Nitrates act as an exogenous source of nitric oxide, which causes vascular smooth muscle relaxation and may have a modest effect on platelet aggregation and thrombosis. Remember, someone having an MI is going to be anxious, in pain, etc.....causing vasoconstriction, the whole goal of giving TX is to reduce MVo2 demand! Do most of you still stick on a NRB at 15lpm on these patients as well? Another Myth that has been passed down through years of old school science and teaching! I will dig up the studies about the coronaries and dilatation, and post them for your reading and education pleasure! Respectfully, JW