15 Walters Llsa Articles

1/7/2015





Bradford L. Walters, MD, FACEP William Beaumont Hospital Oakland University William Beaumont School of Medicine



 

  





Evaluation and initial treatment of supraventricular tachycardia. Mark S. Link, MD N Engl J Med 2012;367:1438-48 This review started with a case presentation and went through the types, diagnosis, EKG patterns of SVT’s.

Sinus tachycardia (ST) is the most common SVT and is typically a physiologic response, rarely > 220, P waves evident, regular. Atrial fibrillation with rapid ventricular response (AF-RVR) is the most common pathologic SVT: ◦ ◦ ◦ ◦

Risk factors = older age, male, HTN, CAD. Can be acute onset in patient normally in NSR. In chronic AF SVT can be more gradual in onset. Ventricular rate – 60-220/min.

 





This year there were 13 articles on 12 topics (1 article was a commentary on another) primarily on cardiac issues. However, process improvement in the ED, ketamine, pain management, and newer anticoagulants were covered. There was at least one “must read” article.

A 24 y/o female with only complaint of “racing heart”, abrupt onset, prior H/O palpitations that resolved spontaneously. VS – 84.60, 190 EKG = narrow complex tachycardia w/o clear P waves. How should this case be managed?

Atrial flutter (Afl) is the 2nd most common SVT: ◦ Due to reentry circuit around the tricuspid valve. ◦ Atrial rate = 280-300, 2:1 block common giving a ventricular rate = 150 (suspect Afl if rate is 150).

Pt. with a run of Afl with variable block that then went into AF with a controlled ventricular response.

1

1/7/2015













Other common etiologies of SVT are:

◦ Atrioventricular nodal reentrant tachycardia (ANRT) ◦ Atrioventricular reciprocating tachycardia (ART) ◦ Atrial tachycardia (AT)



◦ Rates = 150-250. ◦ Ventricular response is regular. ◦ Occur in 1/500 persons in the U.S.



Share a lot of same characteristics:

Also known as reentry tachycardia due to a bypass circuit of cardiac tissue that lacks the usual normal insulation. With antegrade conduction one can see a delta wave in most cases (short PR interval). Both the delta wave and tachycardia defines Wolf-Parkinson-White syndrome.



Typically in patients > 20 y/o. Caused by a reentry loop within the AV node or atrial tissue. Two conduits; one slow, one fast allows for a reentry loop, P waves typically not seen on EKG.





AT is a regular, focal tachycardia due to micro-reentry circuit or automatic focus. Unique characteristics of AT are: ◦ They occur is repetitive short bursts. ◦ Have a warm-up phenomenon of the rate increasing over 5-10 seconds then stabilizing out. ◦ EKG shows a P wave preceding each QRS unless obscured by the T wave if the rate is high.

Less common SVT’s: ◦ Multifocal Atrial Tachycardia (MAT) – requires at least abnormal P waves, due to poisoning of the atria by hypoxia, increase atrial pressure, or theophylline, uncommon, irregular, rate modestly faster than baseline. ◦ Frequent PAC’s – not technically an SVT but morphologically appears similar, irregular, rate = 100-150/minute.

 





Junctional tachycardia – very rare, unusual in adults, can be seen in infants. Paroxysmal junctional retrograde tachycardia – bypass tract near the AV node conducts only retrograde, usually with dilated cardiomyopathy. Wide-complex reentrant tachycardia – occurs with conduction down abnormal atrial tissue and back up the AV node. All of these are so rare it is unlikely to be seen by most practicing ED physicians.

2

1/7/2015



To begin the SVT differential the physician should: ◦ Look at the ventricular response (not atrial) on the EKG. ◦ QRS complex – narrow vs. wide. ◦ Regularity – regular = <10% beat-to-beat variation. ◦ Rapidity of onset. ◦ Heart rate.



Once the QRS is noted to be narrow assess if a P wave precedes it: ◦ ◦ ◦ ◦



Sinus tachycardia. Atrial tachycardia. Multifocal atrial tachycardia. Multiple atrial PAC’s.

P wave follow the QRS:

◦ AV nodal reentrant tachycardia. ◦ AV reciprocating tachycardia.



P waves not apparent:

◦ Atrial flutter with rate > 150. ◦ Atrial fibrillation with rapid ventricular response.

SVT with aberrancy









 





Wide-complex SVT’s are more difficult to diagnose – can be ventricular or supraventricular. Ventricular – VT, VF, torsades, polymorphic VT. SVT with aberrancy or by-pass tract results in a widened QRS i.e. WPW Ventricular sources tend to be irregular while a regular wide-complex tachycardia can be either ventricular or supraventricular.

Vagal maneuvers and adenosine can be useful diagnostically and therapeutically. Slowing of the rate can allow visualization of P or flutter waves and can terminate AVNR and AVT tachycardias. Adenosine blocks AV nodal conduction transiently and can terminate some 80% of atrial tachycardias. Rarely due to exciting atrial and ventricular tissue adenosine can induce AF or nonsustained VT.

Torsades VT







Verapamil, diltiazem are Ca-channel blockers that block AV nodal conduction. Hypotension can be an adverse side-effect so they are not first line medications. Electrical cardioversion is reserved for unstable patients unresponsive to adenosine.

Presenters note: diltiazem is very effective in controlling the ventricular rate with AF/RVR. Unstable = signs of malperfusion including hypotension < 90mmHg, chest pain, cardiac ischemia, cerebral malperfusion.

3

1/7/2015





 



 

 







Adenosine can be useful in wide-complex regular SVT’s – not irregular where it can result in an unstable rhythm. Occasionally adenosine can open up a bypass tract accelerating the ventricular rate. Ca-channel blockers should not be used. Procainamide, ibutilide, lidocaine, amiodorone, and sotalol are all useful in treating widecomplex SVT of ventricular or atrial origin. Cardioversion is often necessary and mandatory in the unstable patient.

Regular SVT’s = ST, AFl, AVNR, AVR, AT. Irregular SVT’s = AF, Afl with variable block, MAT, multiple PAC’s. Sudden onset = AF, AFl, AVNR, AVR, AT. Gradual onset = ST, chronic AF/AFl, MAT, frequent PAC’s. Adenosine is useful diagnostically and therapeutically but should not be used in irregular wide-complex SVT’s.

The current literature has mixed results in regards to epinephrine finding it an independent predictor of mortality, no improvement in survival, and improves likelihood of ROSC. The statistics were pretty dense but one unique variable was a propensity analysis to see the effect of epinephrine used before hospital arrival on immediate and1 month survival.



Stable irregular wide-complex SVT’s are typically: ◦ Atrial fibrillation with aberrancy. ◦ Wolf-Parkinson-White syndrome.





  



 





This article suggests “consultation with an expert is generally required” but I would defer to ones clinical judgment.

Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest.

Hagihara A, Hasegawa M, Abe T, et al. JAMA 2012;307:1161-1168. Prospective observational analysis of 417,188 OHCA’s from 2005-8 in Japan in adult patients. The timeframe included introduction of epinephrine as part of pre-hospital standard resuscitation guidelines.

Using the Japanese National Database information of OHCA patients was collected. Glasgow-Pittsburg Cerebral Performance Category (CPC) assessed cerebral function – 1 to 5 scale of good cerebral performance to death. Overall Performance Category (OPC) assessed neurologic outcome – 1 to 5 scale of no/mild disability to death. Etiology of the cardiac arrest was determined

clinically by the attending physician.

4

1/7/2015



◦ ◦ ◦ ◦ 



ROSC before hospital arrival. Survival at 1 month. CPC category 1 or 2 at one month post-arrest. OPC category 1 or 2 at one month post-arrest.

417,188/431,968 OHCA’s met inclusion criteria, mean age = 72, no demographic differences between epi/no-epi groups. Rate of epi use increased from 190 cases in 2005 to 8,124 in 2008.

EPI

No Epi

18.2%

4.4%

Survival 1 month

3.8%

3.4%

CPC category 1 or 2

0.6%

1.3%

OPC category 1 or 2

0.7%

1.3%

ROSC Pre-hospital





EPI

No Epi

ROSC pre-hospital

21.1%

22.3%

Survival 1 month

15.4%

21.3%

CPC category 1 or 2

6.1%

13.5%

OPC category 1 or 2

6.2%

13.5%

There were 4 end-points:

13,401 patients who receive epinephrine were matched with 13,401 patients who did not. Outcomes remained the same – increased rate of ROSC that did not result in greater survival or function.











VERSUS 

A positive association between epi use and ROSC before hospital arrival was found – O.R. = 1.15. A negative association between epi use and survival at 1 month, CPC, and OPC was found – O.R. = 0.46.

More patients arrived with ROSC who received epinephrine but this did not translate to greater survival or better functional or neurologic outcomes.

IV epinephrine administration was an independent predictor of worse 1month survival in OHCA even after controlling for selection bias with a propensity analysis. Epinephrine use was associated with an increased rate of ROSC but that did not translate into improved outcomes.

This might be due to epinephrine saving the heart but not the brain.

A study with similar results recently was published – Sanghavi BS, et al. JAMA Intern Med doi:10.1000/jamainternmed.2014.5420, published 11/24/2014

5

1/7/2015





  

Questioning the use of epinephrine to treat cardiac arrest. Clifton W. Callaway, MD, PhD JAMA 2012;307:1198-1200. A commentary on the previous epinephrine article by a physician from the U. of Pittsburg Department of Emergency Medicine and Department of Pharmacy.









Epinephrine has a been a mainstay drug in cardiac resuscitation/ACLS since the 1960’s. It has been shown in animals and humans to increase BP and coronary perfusion pressure. When CPR does not generate 1520 mmHg CPP cardiac mechanical activity rarely occurs. Dog studies from the 1960’s established the 1mg dose we still use today. However, experience shows us that ROSC does not correlate always with good outcome.



Raw data of the Hagihara study shows that the administration of epinephrine is associated with:

◦ Increased ROSC (18% vs.. 5%) ◦ Modest increase of survival at 1 month (5.4% vs.. 4.7%) ◦ But a lower rate of good functional status (1.4% vs.. 2.2%)







Both Behringer and Holmberg in 2 observational studies found that an increasing epinephrine dose was associated with worse survival and neurologic outcome (cause and effect?). Gueugriaud and Callaham found additional epi doses over 1mg did not correlate with greater survival even with ROSC. Behringer W, et al. Ann Intern Med 1998;129:450. Holmberg M, et al. Resuscitation 2002;54:37. Gueugriaud PY, et al. N Engl J Med 1998;339:1595. Callaham M, et al. JAMA 1992;268:2267.

When looking at odds ratios particularly with the propensity data better functional status was lower in the epi-treated group (0.210.71).

One theory is that epinephrine creates a supply/demand mismatch where the demand from increased rate and blood pressure on the heart is not adequately met by a compensatory increase in CCP.

DEMAND SUPPLY

Another untoward effect of epinephrine is that it is associated with a greater incidence of arrhythmia that is poorly tolerated post-ROSC

6

1/7/2015













So should physicians stop using epinephrine the the setting of pre-hospital cardiac arrest based on the findings by Hagihara?

“The best available observational evidence indicates that epinephrine may be harmful to patients during cardiac arrest.” The author calls for a rigorously conducted and adequately powered clinical trial comparing epinephrine with placebo.

TH is a clinically-driven treatment modality aimed at reducing core body temperature. Various arguments over precise temperatures for mild, moderate, deep, and profound hypothermia go on. Most authors agree that TH currently targets a goal temperature of 32-34oC post-CPR.



  







 



Therapeutic hypothermia: a state-of-the-art emergency medicine perspective. Varon J, Marik PE, Einav S. Am J Emerg Med 2012;30:800-810. While hypothermia has been used in medicine for centuries only recently has it been shown to increase better neurologic outcomes postCPR. The authors present the history of TH, current applications, and its future.

Use of cold for local therapy dates back to Egyptian times. Hippocrates (460-370 BC) suggested cold water for joint injuries. Galen (130-200 AD) used “cold cream” for fevers. Wm. Osler (1849-1919) lowered the mortality of typhoid at Johns Hopkins from 24.4% to 7.1% by cooling his patients. Temple Fay (1895-1963) stuck cancer patients outside to cool them to 90oF to control pain and showed improved recovery from TBI.

(130AD – 200AD)





Hippocrates (460BC – 370BC)

Sir Wm. Osler (1849-1919)



In the 1950’s TH was being used in cardiac surgery with better neurologic outcomes felt to be due to decreased brain oxygen consumption (pump head). By 2003 the AHA and European Resuscitation Council felt with 2 studies that there was enough data to recommend TH for postarrest patients with ROSC. Those studies from Australia and Europe found better CNS outcomes with TH with the NNT = 7.

Temple Fay (1895-1963)

7

1/7/2015

CARDIAC ARREST LOC in 10 seconds



EEG isoelectric in 20 seconds

◦ Cerebral metabolism decreases 6-7% for every 1oC reduction in core body temperature. ◦ Cell wall integrity enhanced reducing apoptosis. ◦ Inhibits NDMA receptors reducing intracellular Ca. ◦ Improves oxygen supply to ischemic areas. ◦ Decreases ICP secondary to hypothermia induced cerebral vasoconstriction. ◦ May act as anticonvulsant.

Anaerobic glycolysis, energy stores depleted, intracellular calcium accumulation

ROSC

Moderate TH results in:

As core temperature increases NDMA receptors are activated and increases cellular Ca.

Cerebral tissue injury continues with reperfusion due to free radical generation worsened by any 0.5o increase in temperature above 37oC



On the heart TH causes:

◦ Decrease in heart rate, reduces metabolic demand. ◦ Reduced CO ~7% for each 1oC fall in core temp. ◦ Increased SVR so MAP is usually preserved despite the fall in HR and CO. ◦ Concerns for resistance to defibrillation are not thought to be extent in moderate TH, swine data suggests better response to defibrillation. ◦ Ventilatory requirements are reduced, as expected, optimal ABG strategy is not known at this time. ◦ Renal blood flow increases resulting in a cold diuresis and K+ loss. ◦ Platelet function is decreased, bleeding rare.

 









  





Two modalities – surface and invasive. Surface cooling is simpler but achieving target temperature takes longer, 2-8 hours. Surface cooling may not decrease target organ temperature very efficiently. Shivering response is more pronounced with surface cooling and needs to be controlled. Ice packs, cold air or water blankets, or hydrogel pads have all been used.

Invasive cooling have the advantages of cooling the patient faster and more precisely. Cools the core organs better. Less shivering. But is invasive and higher risk, more difficult to institute. Bypass and endovascular cooling catheters are the most commonly used modalities. Typically the catheter is placed in the femoral vein up the inferior vena cava.

8

1/7/2015



















Infusions of iced IV fluids (usually lactated ringers) has been shown to be a means of rapidly instituting TH. Volumes of 2L to 30 cc/kg infused over 30 minutes has been shown to effectively lower the core temperature to ~34oC. Starting cold IV fluids can be done in the prehospital setting though studies have not shown improved outcomes.

A variety of devices and sites (rectal, bladder, esophageal, endovascular) have been used to monitor core body temperature. Pulmonary artery probes are very accurate but difficult to place. Nasopharyngeal or esophageal monitors correspond to brain temperature and the most commonly recommended.

Current recommendation for TH is in an unconscious adult with ROSC after OHCA. Initial recommendations limited TH to postarrest VF patients but now any other rhythm could benefit from TH. Other modalities where TH has been used include TBI, traumatic arrest, meningitis, neonatal hypoxic encephalopathy, near drowning, hepatic encephalopathy, ARDS, and cardiac failure.





The use of TH in traumatic brain injury is gaining more acceptance though the studies are contradicting in terms of outcome. A Cochrane type review suggested that best evidence supports the use of early TH.

9

1/7/2015









Animal models show better neurologic outcomes of an acute CVA with TH. A few pilot studies have shown induction with cold IV fluids is safe. Mild TH to 35oC is well tolerated without shivering in awake patients. No randomized trials have been performed to base a recommendation of TH in acute CVA.









Not an ED issue – ever! Recommendation is no faster than 0.5oC per hour over 24 hours minimum. Shivering often needs to be controlled.

Other complications include: Dysrhythmias Hyperglycemia Coagulopathies Infection, often pneumonia – prophylactic antibiotics are not currently recommended. ◦ All TH patients should receive prophylaxis for DVT’s with at least calf compression devices. ◦ ◦ ◦ ◦





Clearly the earlier the better – time is brain and heart. While no study has shown improved outcomes with invasive over surface cooling the invasive technique cools the patient and core organs faster and more precisely.













 

Shivering – controlled with sedation (midazolam) or anti-shivering agents (meperidine). The author recommends a combination of propofol and remifentanil as they have such short half-lives. Paralysis may need to be initiated, typically using rocuronium.

Ideal TH patient – cardiac arrest with ROSC, VF/VT, hemodynamically stable, unresponsive. How soon? – ASAP, may still benefit 8 hours out. How to induce? – ice packs, cold IV fluids, surface cooling, invasive cooling. Adjunctive meds – sedation, paralysis. Temperature monitoring – continuous bladder, esophageal, rectal, PA.

10

1/7/2015



  



Accidental hypothermia. Brown DJA, Brugger H, Boyd J, Paal P. N Engl J Med 2012;367:1930-1938. Unlike TH accidental hypothermia (AH) is an involuntary lowering of core body temperature (CBT). This is a review article of the physiology and treatment of accidental hypothermia often far below that which is used therapeutically.





 



 











 

Priorities in the field include:

◦ Careful handling to prevent VF. ◦ Basic or advanced life support as the case warrants. ◦ Passive and/or active external warming with warmed IV fluids being effective (38-42oC). ◦ Transport.

Large volumes of fluids can be necessary, but one must be aware that a lot of NS can induce hyperchloremic acidosis. If not signs of life can be detected CPR should be initiated.

The patient is not dead until they are warm and dead.

 





As the body responses to maintain 37oC are exceeded (movement, shivering) energy stores are depleted and core body temperature drops. Consciousness, breathing, circulation become impaired. Confusion at a CBT < 28oC is often seen. AF is common at a CBT < 32oC with a greater risk of cardiac arrest that increases substantially at a CBT < 28oC. Often AH is accidental but numerous diseases can also cause low CBT.

An accurate CBT is necessary. Esophageal probes work well in intubated patients but can be falsely high is using heated oxygen to ventilate the patient. A bladder probe can also work well unless one is doing warm peritoneal lavage. A thermistor probe in contact with the TM is one of the best means of temperature measurement. AH is considered if the CBT is < 35oC.

Patients with impaired consciousness should be assessed for cardiac instability. Stable patients may only require active external warming with minimally invasive rewarming (heating blanket + warm IV fluids). Unstable patients (SBP < 90mmHg, CBT < 28 oC, cardiac arrest) should, if possible, be transported to a facility that can provide ECMO or cardiac bypass warming. Survival with good neurologic outcome has been seen even with CPR that went on for hours (longest CPR with good recovery = 190 minutes).

11

1/7/2015















For the stable patient treatment is relatively easy – continue active external warming, minimal invasive warming with warmed IV fluids. Should central line placement be necessary beware the irritable heart and keep the wire and catheter out of the heart to prevent the potential for arrhythmias. ECMO or cardiac bypass may be necessary for the unstable patient who does not respond to medical management.





 









Vasopressor use in animal models have show mixed results. A modified approach to ACLS with up to 3 defibrillations and holding epinephrine until the CBT is > 30oC. The interval between epi doses should be doubled until CBT is > 35oC. Terminate CPR if remains asystolic with CBT > 32oC.





?

Rescue collapse refers to cardiac arrest related to extrication and transport of a patient in deep hypothermia. Best evidence attributes to either hypovolemia or cardiac arrhythmia. After drop is defined as continue core cooling after rescue seen more in artificial cooling studies. With active external and minimally invasive rewarming this has not been reported.

With no signs of life or vital signs the consensus opinion is to initiate ECMO or cardiac bypass. Survival rates of 47-63% have been reported with initiating this form therapy – without such measures limited data gives a survival rate of only 37%. If such therapies are not available CPR with rewarming should continue. Should ROSC occur expect multi-organ failure and the need for ventilatory support.

High K+ is seen primarily secondary to cell death with an elevated level associated with non-survival. Highest recorded K+ levels in survivors: ◦ ◦ ◦ ◦



11.8 in a 31-month old child 9.5 in 13 y/o child 7.9 in a 34 y/o adult 6.4 in an adult buried an avalanche

Authors recommend terminating resuscitation if K+ > 12 mmol/L and if between 10-12 initiating ECMO/bypass.

12

1/7/2015







Trauma, shock, cerebrospinal injuries can all impair thermoregulation making such patients prone to hypothermia. Clotting factor and platelet activity is reduced, particularly a CBT< 34oC. Transfusions are commonly necessary.



Lowest reported CBT with full neurologic recovery has been: ◦ 14oC accidental ◦ 9oC induced





   

Most common cause of death = pulmonary edema + organ failure. For arrested patients with ECMO the mortality is 50% with full recovery possible if hypoxia did not precede the hypothermia and no serious co-morbidities.

Cardiovascular disasters in pregnancy. Sommerkamp SK, Gibson A. Emerg Clin N Am 2012;30:949-959. A review of pregnancy related heart/lung disasters with the authors out of U. of Maryland Department of Emergency Medicine.









Typically avalanche burial < 30 minutes is not associated with hypothermia. If the airway is obstructed with snow, the victim has been buried > 30 minutes, and is asystolic CPR is unlikely to be beneficial. Cold water immersion without submersion can have a better prognosis even with deep hypothermia and asystole. The record submersion without neurologic impairment to date is 66 minutes in a 2.5 y/o child.











Advances in rewarming with more invasive modalities has improved the outcome in accidental hypothermia. In the stable patient active external rewarming + warmed IV fluids is associated with a very good prognosis. For unstable patients, those not responsive to medical management, or who have arrested ECMO/bypass offers the best outcome. If asystolic once CBT reaches 32oC or the K+ is > 12 mmol/L CPR is considered futile.

Normal cardiovascular changes during pregnancy include: ◦ ◦ ◦ ◦





Cardiac output increase of 50%. Increased blood volume. Increased pulse rate. Decreased systemic vascular resistance.

Such changes are particularly dangerous should the patient have an underlying cardiac problem. Overall pregnancy related mortality is13.95/100,000 pregnancies with 8 cardiac arrests or 1:20,000 maternities.

13

1/7/2015







Venous thromboembolism (VTE) is more common in the pregnant state (1.94/100,000 pregnancies) due to hypercoagulability. D-dimer is less specific as it elevates throughout the pregnancy and its usefulness decreases the later in pregnancy. Adjusted trimester levels proposed by Kline are:



◦ CT – less radiation exposure to the fetus, more to mother (breast tissue). ◦ V/Q – more exposure to the fetus, less to mother. ◦ Both imaging modalities have “acceptable” levels of radiation exposure. ◦ MRI – no radiation, less available, have to lie supine for a longer period of time. ◦ US – no radiation, misses pelvic VTE. ◦ Echocardiogram – excellent adjunctive test, looks for RV strain to Dx submassive/massive PE.

◦ 750 ng/dl first trimester. ◦ 1,000 ng/dl second trimester. ◦ 1,250 ng/dl third trimester.





Treatment: ◦ Traditionally heparin now supplanted by LMWH. ◦ Coumadin is a class X drug, fetotoxic. ◦ TPA – on a case-by-case basis, assume a PE is the etiology of cardiac arrest in a pregnant patient and has been used successfully but often fetotoxic.





Cardiac disease is not that uncommon in pregnant women and accounts 2.27 deaths/100,000 maternities and complicates 1-4% of pregnancies. Obesity, HTN, DM, hypercholesterolemia, and older women having children are felt to account for a rising incidence of cardiac problems during pregnancy.

Imaging becomes problematic:

 

  

2nd most common cause of maternal death. 50% of dissections in women < 40 y/o occur during pregnancy. Diagnosis is challenging and shares the difficulties with VTE/PE – D-dimer non-specific, imaging problematic. TEE is ideal if available. CT delivers a lot of radiation and dye. Treatment is the same an in non-pregnant woman, betablockers felt to be safe.

Risk Factor

Pregnant, morbidly obese at baseline , diabetic, hypertensive and 38 years old – oh, perfect!

Points

NY Heart Association Class II-IV ht. failure or cyanosis

1

Previous cardiac event (CVA, TIA, ACS) or arrhythmia

1

Left heart obstruction (MV area < 2cm2, AV area < 1.5cm2, LV outflow gradient > 30mmHg

1

Ejection fraction < 40%

1

14

1/7/2015







Valvular disease, infectious or congenital, places a pregnant patient at risk particularly with mitral/aortic stenosis. Cardiomyopathy is typically viral in etiology but can be infectious, of particular risk if the ejection fraction is < 40%. Have a high level of suspicion for cardiomyopathy in the pregnant patient complaining of dyspnea, fatigue, pedal edema

(challenge being is all pregnant patients complain of those symptoms). 

BNP can be helpful with 100-300 pg/ml indicating cardiac disease and >300 indicating overt CHF.



Usually palpitations are benign but more serious arrhythmias have to be ruled out. SVT’s are common and adenosine can be used safely, rate control for AF/RVR, and cardioversion as in a non-pregnant patient. Cardioversion is safe in all trimesters, sedation is more risky in the 3rd trimester because of potential hypoxia or aspiration. LMWH is the anticoagulant of choice.



Reversible causes:







◦ Hypovolemia – blood loss, DIC, placenta abruption or previa. ◦ Vasodilatation – septic shock, thyroid storm. ◦ Pump failure – cardiomyopathy, AMI, arrhythmia. ◦ Outlet obstruction – pericardial tamponade, PE. ◦ Should ROSC occur hypothermia is being recommended more and more with one case report of a favorable outcome for the mother and fetus. 

If perimortem C-section is best if considered within 4 minutes of onset of cardiac arrest.





















Management of cardiomyopathy in pregnancy is as usual save for no ACEI/ARB’s. AMI is 3-4x more common in pregnant than in non-pregnant women. Management is the same – ASA, betablockers, nitrates, PCI. Clopidogrel (Plavix) is considered safe but can cause excess bleeding at delivery. ACEI/ARB’s, statins are contraindicated.

Cardiac arrest can have a number of different etiologies with PE and primary cardiac being the most common. Compression on the aorta and IVC by the gravid uterus has to be relieved with pushing the uterus to either the right or left. The usual ABC’s should be changed to “CAB”, medications and defibrillation as usual per ACLS. Consideration of TPA for a massive PE if the patient remains unresponsive.

Reversible causes – H&T’s           

Hypovolemia Hypoxia Hydrogen ions (acidosis) Hyper/hypokalemia Hypothermia Hyper/hypoglycemia Tablets/toxins/OD Tamponade – cardiac Tension pneumothorax Thromboembolism (PE) Trauma

15

1/7/2015



       

   

Bleeding/DIC Embolism Anesthetic complications Uterine atony Cardiac disease Hypertension/eclampsia Other Placental abruption/previa Sepsis

Coronary CT angiography versus standard evaluation in acute chest pain. Hoffman U, Troung QA, Schoenfeld DA, et al. N Engl J Med 2012;367:299-308. A mulitcenter trial where patients with symptoms suggesting ACS without ischemia on EKG or a positive troponin were randomized to early CCTA or standard evaluation during weekdays.



   















Between 4/2010 and 9/2012 patients presenting at 9 different hospitals during the week and in daytime hours with chest pain or symptoms suggesting CAD between the ages of 40-74 years old. Patients were randomized to CCTA or the standard CAD evaluation at that hospital. Exclusion criteria were patients with known CAD, evidence of ischemia by EKG or labs, unstable, obese, or allergic to dye.







Cardiovascular emergencies in the pregnant patient while not common are not uncommon. They tend to be devastating and can be difficult to diagnose and treat. The best chance for the fetus is to take care of the mother. Keep in mind PE, decompensated CHF, AMI, arrhythmia. Most often the therapeutic approach is similar if not the same as it the non-pregnant patient.

CCTA has been shown to have a high sensitivity and specificity for the detection of clinically significant coronary artery disease. Normal findings have a very high negative predictive value in low risk patients. It is suggested that CCTA can rule out significant CAD faster and with less radiation than stress myocardial perfusion studies. This study looked at a 64-slice CCTA compared to a standard evaluation for CAD.

Primary endpoint – hospital length of stay (LOS). Secondary endpoints – time to diagnosis, rate of direct discharge, resource utilization, cumulative radiation exposure, 28-day follow-up. 1,273 patients assessed, 1,000 randomized, 501 CCTA, 499 standard evaluation, 99-98% were followed up at 28 days.

16

1/7/2015



 















End Point

Of the 501 randomized to the CCTA group 28 did not get the study for one reason or the other. 75 patients (8%) had a final diagnosis of CAD. Agreement for discharge between the site and an independent panel was high (kappa = 0.94). Average LOS was 7.6 hours less for the CCTA group with 50% discharged within 8.6 hours compared to only 10% of the standard group in that timeframe, mean time to diagnosis was much less for the CCTA group.

No cases of undetected CAD were identified in either group. There were 8 major cardiac events at 28-day follow up in the standard group, 2 in the CCTA group. Of those 2 patients in the CCTA group significant CAD was identified but both had negative stress tests and were treated medically.

This study looked to see if early CCTA in the work-up of low risk chest pain safely improved the efficiency of clinical decision making compared to standard evaluations. The average LOS was significantly reduced with a high proportion of CCTA patients directly discharged from the ED without a greater risk of undetected CAD. There were no cases of missed CAD in either group.



CCTA

Standard

LOS – all patients

23.2 hours

30.8 hours

LOS – patients w/o final Dx of CAD

17.2 hours

27.2 hours

LOS – patients with final Dx of CAD

86.3 hours

83.8 hours

Time to Dx – all patients

10.4 hours

18.7 hours

Time to Dx – patients w/o final Dx of CAD

10.6 hours

18.8 hours

Time to Dx – patients with final Dx of CAD

8.0 hours

17.1 hours

In the CCTA compared to the standard group:

◦ More diagnostic testing. ◦ Non-significant higher rate of eventual revascularization. ◦ Higher radiation exposure as only 33% patients in the standard group received any radiation exposure at all compared to 100% of the CCTA group. ◦ Costs overall were similar between the groups.





The CCTA group ended up with more invasive coronary procedures as more CAD was detected that had to be addressed and at a cost of more radiation exposure to the group overall. There was no reduction in costs seen with the use of CCTA despite its overall greater efficiency.

17

1/7/2015

  



Infective endocarditis.



Hoen B, Duval X. N Engl J Med 2013;368:1425-1433. A review of infective endocarditis (IE) starting with a case presentation.







 





Strep and Staph account for 80% of IE. With increase in health-care associated disease Staph IE is on the rise. Culture negative IE (~10% of cases) is felt to be due to the patient getting Abx’s or fastidious organisms (PCR or serologic testing can help) i.e. bartonella, brucella, Q fever, HACEK group of bacteria (haemophilis, Aggregatibacter, actinomycetemocomitans, Cardiobacterium, Eikenella, Kingella). Oral strep is less common now with prophylaxis.



Strep pneumoniae

  

Annual incidence – 3-9 cases/100,000 persons in industrialized countries with a 2:1 male to female ratio. Risk factors – prosthetic valves, intracardiac devices, unrepaired congenital heart defects, and a history of IE in the past. Other factors – valvular lesions, hemodialysis, DM, immunodeficiency, HIV, IVDA. ~33% due to be due to health-care associated bacteria.

Normal valve endothelium is resistant to bacterial invasion unless the tissue is damaged by jet lesion or inflammatory disease. Solid infective particles from IVDA can both injury the valve and colonize it. Old classification was based on rapidity of onset. Now the classification is based on underlying cardiac conditions, location, presence of intracardiac device, or mode of acquisition.

MRSA



Mortality:



◦ Overall in-hospital mortality – 15-22%. ◦ 5-year mortality – 40%. ◦ Right-sided lesions, oral strep, or left sided native valve lesions in-hospital mortality – 10%. ◦ Prosthetic valve Staph aureus IE in-hospital mortality – 40%+. ◦ Risk factors for death:     

Older age S. aureus IE Heart failure Cerebrovascular and embolic events Health-care associated IE

Diagnosis rests on clinical, microbiological, and echocardiographic findings with the definitive diagnosis =

microorganisms identified by culture or histologic examination of vegetations, intracardiac abscess, or embolic specimen. 

Duke criteria has sensitivity/specificity of 80%.

18

1/7/2015



 

Fever is present in 80%. A new or worsening murmur in 48% and 20%. Less common findings: ◦ ◦ ◦ ◦ ◦ ◦



Janeway lesions are small, erythematous, non-tender, nodular lesions on palms or soles due to septic embolic causing microabscesses.

Hematuria in 25%. Splenomegaly in 11%. Splinter hemorrhages in 8%. Janeway lesions in 5%. Roth’s spots in 5%. Conjunctival hemorrhages in 5%.

Splinter hemorrhages are tiny blood clots seen in the nail beds, usually plum colored, seen in IE.

Labs show an elevated ESR/CRP, leukocytosis, anemia in ~ 50% of cases.

Roth’s spots are retinal hemorrhages often with a pale, white center first identified in 1872 felt to be coagulated fibrin and platelets seen with IE.

Osler nodes are painful lesions on palms or soles seen in IE made up of immune complexes.





 









Cerebral complications are the most severe extracardiac problems with IE. They include ischemic or hemorrhagic CVA, TIA, mycotic aneurysm, brain abscess, or meningitis. 60% of IE associated CVA/TIA’s precede the actual diagnosis. Large, mobile, S. aureus mitral valve lesions impart the greatest risk of embolizing. CT/MRI are the tests of choice.

Identifying the causative organism is key with 3 blood cultures finding the agent in 90%. If cultures are negative serologic testing for bartonella, brucella, and C. burnetii as in-patient. TEE and transthoracic echocardiograms reliably demonstrate valvular lesions showing vegetations in 90%, regurgitation in 60%, and paravalvular abscess in 20%.





 Ruptured mycotic aneurysm from IE.

 







Abscess just above the mitral annulus with a dilated LV secondary to S. aureus IE.



Criteria – 2 major, 1 major + 3 minor, 5 minor = infective endocarditis. Major Clinical Criteria – BC positive x 2, echocardiographic evidence of vegetation, new valvular regurgitation. Minor Clinical Criteria – Risk factor for IE or IVDA, fever, vascular complications i.e. embolus/aneurysm/Janeway/, immunologic phenomenon i.e. Osler nodes/Roth spots, or blood culture positive without major criteria.

Antibiotics are key ranging from 2-6 weeks. For native valves a beta-lactam Abx + aminoglycoside is a good starting choice (Rocephin plus gentamycin). For prosthetic valves infected by staph the same choice of antibiotics with the addition of rifampin if the bacteria is susceptible. Gentamycin is the most evaluated aminoglycoside and should be used until sensitivities are back, how often to give gentamycin is a matter of debate and can be decided outside of the ED. For MSSA gentamycin is not recommended as it does not offer better clinical benefit but is advised with MRSA for the first 2 weeks. Daptomycin is gaining popularity as an alternative to vancomycin in PCN allergic patients.

19

1/7/2015







Early valve replacement is becoming more common, even during the Abx course, ~50%. Indications include heart failure, uncontrolled infection, and prevention of emboli. In the case of an embolus that has already occurred the risk of surgery has to be balanced with the risk further emboli.













Duration of antibiotic treatment continues to be debated particularly with the aminoglycosides along with the role of oral therapy. Surgery timing also remains an area of debate. The treatment of unruptured mycotic aneurysms is uncertain as Abx therapy can resolve them though endovascular treatment for large ones is advisable.

Surgery is indicated for heart failure, uncontrolled infection, and to prevent emboli. Treatment with antibiotics with a starting choice of a cephalosporin plus gentamycin until sensitivities come back, the addition of rifampin initially with a prosthetic valve is reasonable. Prophylaxis is now confined to patients with previous IE, prosthetic valve, or unrepaired congenital heart lesion.



  









 



  

Oral anticoagulants are not recommended even with prosthetic valves due to the risk of cerebral hemorrhage. Heparin for the first 2 weeks is used. Antiplatelets are not recommended. Current prophylaxis for IE is now restricted to patients with a prosthetic valve, h/o IE, or unrepaired congenital heart defect. In Great Britain prophylaxis is not used under any circumstances.

Staph and Strep account for 80% of IE with staph currently the most common. Cerebral complications are the most common extracardiac complications and the most severe. Large, mobile lesions of mitral valve due to Staph are at the greatest risk of embolus. At least 3 blood cultures are necessary. When IE is suspected echocardiography ASAP with both TEE and transthoracic advised.

Lean thinking in emergency departments: a critical review. Richard J. Holden, PhD. Ann Emerg Med 2011;57:265-278. This was a not particularly useful review* of the Lean process of improvement first developed by the Toyota Production System.

*Author’s note: it reminded me of why even as a sociology major I got out of the social sciences .

20

1/7/2015















Lean thinking came out of the auto industry and has spread to many different industries with some 50% of ED’s using this to improve processes. It looks to reduce waste, involve front-line workers, and have continuous rapid improvement sessions (kaizen). This review looked to focus on the ED, how Lean affects ED employees and patients, looks at previous studies for desirable and undesirable effects, analyze Lean’s variability in its success, and analyzes previous studies with an analytical framework as opposed to a narrative story.

The analytic framework yielded 6 questions:

◦ How does Lean transform work structures and processes? ◦ How does Lean affect patient care? ◦ How does Lean affect employee working conditions? ◦ How does Lean affect employee outcomes directly? ◦ How are employee and patient effects of Lean linked? ◦ How are patient care and employee effects of Lean contingent on the organization implementing Lean and features of the design and implementation of Lean?

Table 2 and Figure 3 in the article ran down a large laundry list of changes and results from decreased LOC to improved patient satisfaction to decrease time to doctor. Various process changes established new standards for performance, data collection, and monitoring systems. A number of salutary changes to patient care were evident though changes in overall health outcomes were not studied nor patient safety measures were looked at in only one study.



The studies selected were analyzed according how Lean affects the process of ED work. ◦ Structure – refers to work system elements including tools, technology, worker factors (education, training, responsibilities), organizational factors (policy, staffing, incentives), and physical environment. ◦ Process – the activities involving patient care and flow of the patient through the ED.



  





Also looked at not just employee effects on Lean but how Lean effected the employees themselves.

18 articles involving 15 ED’s included. ED’s tended to be large, teaching hospitals. All involved frontline staff in some way, i.e. suggesting/implementing/designing changes. Most cases Lean was the only change process used – did not compare different approaches. Analysis typically followed the change process where bottlenecks, waste, or other problems were identified and redesign suggested (“changes

were evaluated and adjusted in an iterative way”).







Indirect changes of Lean were not often measured but some evidence of less staff aggression, more courtesy, greater job satisfaction, better retention were mentioned. Direct effects of Lean were seen in employees being more aware of their work, new values, more eager to accept change, and more control of their work. No study looked at Lean related patient and employee outcomes.

21

1/7/2015







In the 5 years since Virginia Mason Medical Center published their landmark experience with Lean many ED’s have used it to assess and change their work environment to address errors, delays, and crowding. Patient care typically improved with these efforts while direct links between Lean and safety have yet to be shown they are implied (i.e. less crowding is known to be associated with fewer medication errors).

The authors offer 9 suggestions regarding Lean: ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦





 

Be ready for change. Take a human-centered approach. Secure expertise. Obtain top management support and resource allocation. Secure leadership. Aim for culture change. Adapt Lean to the local context. Improve continuously. Learn from previous experience.

Relief of pain and anxiety in pediatric patients in emergency medical systems. Fein JA, Zempsky WT, Cravero JP,

The Committee on Pediatric Emergency Medicine and Section on Anesthesiology and Pain Medicine. Pediatrics 2012;130:e1391-e1406. An extensively researched summary to create a systematic approach to pediatric pain management in the emergency setting.



 

  

 



Typically the use of Lean was not directed to improving the employee work environment and only one study measured job satisfaction related to Lean change initiatives. The authors note Lean can increase workload, threaten autonomy, and create anxiety. Some of the research effects of Lean suffers from a Hawthorne Effect, i.e. employees were more satisfied because Lean forces more attention on them and their work environment.

Lean is a process to implement change that has been widely adopted in many ED’s. Typically it has favorable effects. The link between Lean and effects on patient safety, quality outcomes, and on employees is not well known. Factors that contribute to Lean’s success are also not well defined. Employee engagement was typically improved and often ED’s find they cannot go back to old ways of doing things following Lean implementation.

Pain management varies with the age of the patient with numerous barriers in the ED: Difficulty in assessing pain in young children. Unfamiliarity with new techniques and drugs. Fear of adverse effects. Time and staffing limitations in busy ED’s. Misconceptions about masking symptoms that prevent accurate diagnoses. ◦ Physician and parent biases. ◦ Ethnic and socioeconomic variations in analgesic administration. ◦ ◦ ◦ ◦ ◦

22

1/7/2015

There is evidence that minor procedures (needle sticks, IV starts, heel sticks) can affect a child’s long term emotional well-being. Best evidence in neonates is with more effective procedural pain management there are better outcomes. Pediatric oncology patients report higher pain scores when their pain is invalidated by health-care personnel. Do not forget the Joint Commission that mandates the right of all patients to have their pain assessed and managed.















Authors emphasize a pediatric environment with colorful walls, toys, games, video/TV devices to distract patients are important to minimize fear – a major contributor to the pain experience. They also tout the child life specialist who is trained to assess and manage anxiety and pain with distraction techniques, imagery, education, and coping plans. Family presence during procedures can also be helpful in reducing pain.



Presenters total unscientific, non-controlled, non-randomized convenience sample of pain scores (3 weeks ago):







Effective and safe pain management can begin with EMS providers. Adult and 1 pediatric trial showed that opiates and tramadol can decrease pain scores without causing respiratory depression. Transmucosal delivery systems can be particularly easy and effective to use in the prehospital setting.

  



Topical anesthetics can be used to control the pain of IV catheters: ◦ More rapidly acting agents; EMLA, liposomal lidocaine cream, heat activated systems, sprays. ◦ Intradermal injection; benzyl alcohol, buffered lidocaine.

◦ Children < 3 y/o, in ED for medical problem,

parents responding, N = 8 – pain score average = 10. ◦ Prompt care, mix of adults and adolescents, mix of primarily limb injures, N = 12, average pain score = 13.66 (two were > 10). ◦ Adult side, illness, non-trauma, N = 10, average pain score = 8.5.

The Joint Commission has mandatory rules for pain assessments in the hospital. Usually some form of age appropriate pain scale is used. There is question as to the utility of such scores let alone basing the quality of care on them – most patients rate their pain in the ED at 10 and the issue of a statistically significant change in pain scale rating being clinically relevant.

  

Topical anesthetics for laceration repair placed at triage; LET/XAP, EMLA. Use of tissue adhesives and absorbable sutures to avoid having to remove sutures. Buffered lidocaine reduces the pain of injection.

23

1/7/2015







Sucrose has been found to decrease to discomfort of heel sticks, injections, vaccinations with the best evidence in neonates. Skin-to-skin contact and breast feeding also has been shown to decrease discomfort. Elimination of heel sticks and IM injections as IV starts has been shown to be less painful. Pain scores for venipuncture in neonates







There has been in the past great theoretical concern that analgesic administration has the potential to alter that ability to clinically assess a patient – particularly abdominal pain.

Just tell me what the CAT scan showed

There is no evidence that altering the level of pain impairs that clinical assessment.

To a large extent imaging (CT scan) has replaced that icky task of actually getting a history, doing a physical exam, and talking to a patient for general surgeons.







In children with developmental issues pain management can be particularly difficult in the prehospital setting. Pain modulation vary widely related to neurotransmitter alterations in the brain or spinal cord alters but does not preclude pain perception. Ascertaining the degree of discomfort in children who cannot communicate is difficult.







Optimal pain management requires expeditious assessment and rapid administration of an opiate – IV or transmucosal can be useful in the prehospital and ED setting. Pain versus anxiety is particularly difficult to separate in younger children – if a procedure is expected to painful analgesics should be used, anxiety provoking sedatives might be more appropriate. Nitrous oxide is very effective but contraindicated in pneumothorax, bowel obstruction, intracranial injury, and cardiovascular compromise. ED Nitrous Oxide analgesic delivery system





  

Personnel who administer sedation and analgesic for procedures must be able to manage the pediatric airway. A study of 131,751 elective pediatric sedations found no difference in adverse events between anesthesiologists and pediatric medical subspecialists. A separate person monitoring the patient is felt to be essential. NPO guidelines are controversial with insufficient data to determine safe NPO times. The urgency of the procedure is paramount.

24

1/7/2015









  







Training and education in pediatric pain assessment and management should be provided to all EMS personnel. Child life specialists can be valuable adjuncts in non-pharmacologic techniques to reduce pain along with family involvement. Pain assessment begins in the prehospital setting and follows through to the ED and instructions to family on discharge.

Clinical practice guideline for emergency department ketamine dissociative sedation:2011 update. Green SM, Roback MG, Kennedy RM, Krauss B. Ann Emerg Med 2011;57:449-461. This is a comprehensively researched summary of the literature on ketamine by two of the leading lights in ketamine and sedation in emergency medicine (Green, Krause).

Ketamine disconnects the thalmocortical and limbic systems isolating the CNS from outside stimuli. The dissociative effect is seen at doses:

IV 1-1.5 mg/kg IM 3-4 mg/kg In smaller doses it is analgesic and disorienting Once the dissociation threshold is reached additional doses of ketamine does not deepen that effect and are unnecessary. ◦ At these doses there is no clinically important effect on airway integrity, respirations, or blood pressure. ◦ ◦ ◦ ◦

The dissociative state created by ketamine is not a general anesthetic state by all definitions.













 

The administration of analgesics should be an painless as possible. Neonates and young infants should receive adequate pain prophylaxis for procedures. Analgesia does not preclude the clinical assessment of pediatric patients. Sedation and dissociative agents should be provided by appropriate trained personnel and full monitoring should be instituted.

Ketamine is the most popular agent for pediatric procedural sedation with clinical practice guidelines in 1999, updated in 2004, and was felt to be due for another update. Ketamine is sufficiently different from other sedatives in its dissociative effect that it warrants a separate guideline and consideration.

MEDLINE search of the literature 2003-2010. Strength of scientific evidence adapted from the American Society of Anesthesiology: ◦ Supportive – compelling association of clinical intervention and clinical outcome. ◦ Suggestive – enough information from a single study or report to support the intervention and clinical outcome. ◦ Inconclusive – studies exist but cannot provide a clear causal interpretation. ◦ Insufficient – to few studies to support a conclusion. ◦ Silent – no studies to address the relationship in question.

25

1/7/2015



 

“The literature is strongly supportive of the safety and efficacy of ED dissociative sedation for a variety of brief painful or emotionally disturbing procedures in both children and adults.”

Very useful in mentally impaired children. Can be safely used for longer procedures but for something that requires the patient to be motionless (CT, MRI) the random movements with ketamine can be a disadvantage.





Risks may outweigh benefits:

◦ Age – previous guidelines suggested ketamine should be avoided in children 3-12 months, large meta-analysis does not support this and global evidence suggests minimal to no enhanced risk. ◦ Laryngeal Stimulation – ketamine preserves and can exaggerate airway reflexes increasing the risk of laryngospasm with stimulation of the oropharynx, large meta-analysis failed to corroborate an increased risk in typical ED procedures (intraoral laceration, dental procedures, foreign body) though efforts to keep secretions/blood out of the oropharynx is prudent.



Risks essentially always outweigh benefits:

◦ Age - < 3 months there a anecdotal reports of airway complications with ketamine (no different than any sedative) likely due to age specific airway anatomy and laryngeal excitability. ◦ Mental State – ketamine can exacerbate schizophrenia and should not be used on such patients, the literature is silent on other forms of psychosis.



Risks may outweigh benefits: ◦ Anatomy – Inconclusive data on the use of ketamine in patients with tracheal surgery, stenosis, tracheomalacia but such conditions may confer higher risk. ◦ Upper airway infection – some indirect evidence that with an active URI there could be a higher risk of laryngospasm in children not adults, there were some anecdotal cases in the 1970’s and that admonition was listed in all guidelines on ketamine ever since though there is insufficient evidence of this.

Risks may outweigh benefits: ◦ Asthma – while ketamine has been used for therapy for asthma its safety in sedation is not known and active asthma is a known risk for laryngospasm, in quiescent asthma there is no contraindication. ◦ Laryngospasm – ketamine associated laryngospasm is rare (0.3% risk is a large metaanalysis), transient, and responds to assisted ventilation and oxygen.

The infants airway is: - smaller so secretions easily obstruct the opening. - the tongue is larger in proportion to the mouth. - Pharynx is smaller and cone shaped. - Epiglottis is larger and floppier. - narrowest at cricoid. - trachea is narrower and less rigid.



Risks may outweigh benefits: 





Cardiac disease – widely recommended that ketamine be avoided in CAD in both children and adults, its sympathomimetic effect increases BP and pulse mildly but evidence is inconclusive regarding if this increases oxygen demand. The literature is silent on the maximum age for ketamine though millions of older adults have received ketamine safely worldwide over the past 40 years. In addition, the literature is silent on ketamine’s use in patients on OTC sympathomimetic (pseudoephedrine) so these meds do not represent a contraindication.

26

1/7/2015



Risks may outweigh benefits: ◦ Increased ICP – probably no other unverified caution to the use of ketamine has persisted in the literature more than not using it in head trauma or suspected increased ICP, newer data indicates what increase there might be is minimal assuming normal ventilation and ketamine’s vasodilatory effect might actually improve cerebral perfusion.







Irrespective of age the more comorbidities a patient has the greater the risk of adverse events with benzodiazepines, opiates, inhalational anesthetics, and propofol. However, no such association has been shown with ketamine in children and given its supportive cardiopulmonary effects is likely the preferable agent for sedation.

IV route: ◦ Minimum dissociative IV dose is 1.5mg/kg with recommended loading dose of 2mg/kg. ◦ Repeat doses of 0.5-1mg/kg as needed. ◦ IM route:  Minimum IM dose to reliably induce dissociation is 45mg/kg.  Repeat half or full dose as needed is typically effective if needed in a longer procedure.















Risks may outweigh benefits:

◦ Sz disorder – though the literature is silent on this ketamine does have anticonvulsant properties. ◦ Increased IOP – inconclusive and conflicting evidence regarding ketamine increasing intraoccular pressure and should be used with caution. ◦ Thyroid ds., Porphyria – inconclusive data regarding ketamine’s sympathomimetic effect in thyroid and porphyria patients, use caution. ◦ NPO status – there is no data to correlate NPO status with adverse events with ketamine, in 40 years of use and a large ED study showed no association between fasting and adverse events.

Unlike almost any other drug ketamine does not show dose-related increase in adverse events save once IV doses exceed 2.5 mg/kg or 5 mg/kg total dose showing more vomiting and recovery agitation. There is no apparent benefit to using IV 1mg/kg vs.. 2mg/kg or IM 3mg/kg over 4mg/kg. Even data from the 1970’s with doses of 715mg/kg by anesthesiologists showed no increase in adverse events over standard doses.

Anticholinergics – in the past it was recommended to coadminister atropine or glycopyrolate but a meta-analysis showed this is typically unnecessary, can increase airway events but decrease vomiting. Benzo’s – 2 meta-analyses showed prophylactic administration to prevent recovery agitation failed to show a benefit, such reactions are readily ameliorated with titrated benzodiazepines. Antiemetics – prophylactic ondansetron does reduce recovery emesis, NNT = 13.

27

1/7/2015









 



  

 

Laryngospasm – occurs in 0.3%, occurs more with higher doses IV, typically transient with need for BVM/intubation very rare, could be increased with active asthma but not with oral procedure/age/route/coadministered meds. Respiratory depression – very unusual with ketamine save if given rapidly. Emesis – early adolescence is peak age, more with IM route, typically late recovery stage, decreased by Zofran.

Adult use – existing evidence supports the safety and efficacy of ketamine in adults and it is used worldwide (save in the US); more rigorous studies would be helpful. Ketofol – several ED studies show this combination to safe and effective. Neurotoxicity – in animals accelerated nerve cell apoptosis with high doses has been seen but is in complete odds with the human data. Subdissociative doses – used for analgesic, may reduce opiate use.

The prophylactic use of anticholinergics or benzodiazepines is unnecessary. Recovery agitation is unusual and treatable with titrated benzodiazepines. Ondansetron (Zofran) can reduce ketamine emesis that is typically seen in the recovery stage. Safe and effective use in adults has been demonstrated. Like any sedative/analgesic used for procedures careful patient selection and monitoring ensures safe use







 



  

Recovery agitation – hallucinations but unpleasant and pleasant are legendary with ketamine, rarely disturbing in children, occurs in 1.4% in kids and 0-30% in adults, the ED experience is that is uncommon and mild for adults, easily treated with benzo’s. In a large meta-analysis in children this was not related to age, dose, adolescents were not at greater risk, higher incidence with subdissociative doses (<3mg/kg IM).

Ketamine has been shown to be a safe and effective sedative for painful procedures in a wide-variety of ED settings in children and adults. Dissociative doses are IV 2mg/kg, IM 4mg/kg. Most of the concerns with ketamine have not born out in studies and closer scrutiny including recovery agitation is older patients, increased ICP, cardiac risk, and laryngospasm with oral procedures.

Electrocardiogram findings in emergency department patients with syncope. Quinn J, McDermott D. Acad Emerg Med 2011;18:714-718. A study of consecutive ED patients with syncope to determine the sensitivity and specificity of the San Francisco Syncope Rule (SFSR) to predict at risk patients of a cardiac problem.

28

1/7/2015







Syncope is a transient LOC and postural tone followed by spontaneous recovery accounting for 1.2% of ED visits. By far the usual causes are benign, typically vasovagal however, 5-10% have more serious etiologies with significant mortality. Because of that a large number of patients are admitted (5085% in the U.S. compared to 1530% in Canada and Australia) with a cost of $2 billion/year.





Some dated cost data on some common tests done to ascertain the etiology of syncope. Gives a sense on how this could cost $2 billion particularly when some 85% of patients who present to the ED with syncope are admitted in the U.S.

Numerous studies looking to derive predictors of serious etiologies with the EKG consistently one of the major determinants. However, studies vary on what is an “abnormal” EKG, in the derivation of the SFSR it was any non-sinus rhythm on EKG or

monitoring. 







In that study cardiac and non-cardiac serious outcomes were lumped together and did not specify which EKG findings were abnormal.

This study was an analysis of a previous database to determine the sensitivity for the EKG criteria of the SFSR for cardiac outcomes. The initial prospective study was from 20002002 and this reanalysis was blinded to the initial assessment, looked only at cardiac outcomes (sudden death, AMI, arrhythmia). Abnormal EKG’s included rhythm abnormalities (SVT, VT, blocks, paced), RBBB, LBBB, ST changes, non-specific ST changes, PR/QT interval changes, ectopy, Q-waves.

684 consecutive patients considered 634 had EKG and rhythm analysis completed 42 (6%) suffered cardiac outcome

EKG criteria predicted 36 of 42 patients with cardiac outcomes

Sensitivity = 86%

Specificity = 70%

Negative predictive value = 99%

29

1/7/2015







  







Specific EKG findings:

◦ Isolated LBBB, any LBBB (partial or complete) were associated with serious cardiac outcomes. ◦ Q-waves, RBBB, ST segment changes, NSR were not associated with serious cardiac outcomes. ◦ On a separate rhythm analysis a significantly greater number of patients had non-sinus rhythms that what was just seen on EKG (72% vs.. 34%).

Any non-sinus rhythm, any LBBB, any left bundle conduction problem (LAHB, LPHB, QRS widening) were 2.8-3.2 times more likely to have a significant cardiac outcome.

New oral anticoagulants in the ED setting: a review. Charles V. Pollack, MD Am J Emerg Med 2012;30:2046-2054. A general review of the new OAC’s coming into use for treatment of VTE and stroke prophylaxis in AF and their adjunctive use with antiplatelet agents for ACS patients.

Warfarin, LMWH, fondaparinux all have a lot of interpatient variability due to genetics, a very large number of drug-drug and drug-food interactions, need frequent monitoring, and bleeding with coumadin the most frequent cause of drug-related admission in older patients. The NOAC’s have 2 classes; direct thrombin inhibitors, selective factor Xa inhibitors. They are more bioavailable, have little drug-drug and drug-food interactions, have less associated bleeding, do not need monitoring.

  





In the SFSR (and any other syncope rule) the EKG plays a key role to determine risk. That risk was very low in patients with a normal EKG. Any non-sinus rhythm confers a 2.8 times greater risk of a serious cardiac outcome, the EKG may miss a significant number of nonsinus episodes picked on rhythm analysis. Any LBBB or left bundle conduction abnormality confers a 3.2 times greater risk of a serious cardiac outcome.

Novel oral anticoagulants (NOAC’s) have indications for: ◦ Prevention and treatment of VTE. ◦ Stroke prophylaxis in non-valvular AF. ◦ Acute coronary syndrome.





They replace the traditional LMWH or UFH followed by long-term vitamin K antagonists (VKA) for VTE and long-term VKA for stroke prophylaxis in AF. The newest paradigm is the addition of the NOAC’s to antiplatelet agents long-term after ACS.

Factor Xa Inhibitors -Rivaroxiban (Xarelto) - Apixaban (Eliquis)

Thrombin Inhibitor - Dabigatran (Pradaxa)

30

1/7/2015





Acute VTE Treatment:

◦ Patients with proximal DVT’s or PE’s who required 6 months of anticoagulation had similar recurrence rates compared to coumadin (2.4% and 2.1%) with significantly less bleeding.

Acute VTE Treatment: ◦ Patients with either proximal DVT or extensive calf DVT apixaban compared to coumadin showed similar recurrence (4.2% vs.. 4.7%) and bleeding rates (7.3% vs.. 7.9%).











For secondary VTE prevention a trial is currently in progress but has yet to be indicated for prophylaxis.

In the RE-LY study dabigatran 150mg BID (75mg BID if CrCl is 15-30 ml/min) reduced the risk of stroke and embolism in non-valvular AF by 1.53%/year compared to coumadin at 1.69%/year. Rates of ICB were lower in the dabigatran group as was the incidence of intracranial bleeding. A greater rate of stomach upset was seen with dabigatran. The rate of AMI was also higher with dabigatran.

Acute VTE Treatment: ◦ Compared to coumadin the DVT recurrence rates were 2.1% vs.. 3.0% with similar major/non-major bleeding. ◦ For PE compared with coumadin recurrent VTE was similar with less bleeding with rivaroxaban.

Secondary VTE Prevention:

◦ Patients who had 6-18 months of anticoagulation who needed continue therapy for another 6 months had a minimal recurrence rate (0.4%) compared to placebo and in another trial had a similar recurrence rate to coumadin (1.8% vs. 1.3%) again with much less bleeding (0.9% vs. 1.8%).







Secondary VTE Prophylaxis: ◦ For DVT or PE after 6-12 months with either placebo or rivaroxaban showed a lower recurrence rate (1.3% vs.. 7.1%) for rivaroxaban and a bleeding rate of 6%.



  







AF affects 1-2% of the general population expected to increase 2.5x as the population continues to age. Paroxysmal AF confers a 5x increased risk of stroke. With coumadin there is a 68% relative risk reduction, 21% for ASA. The NOAC’s are also being used in AF not associated with prosthetic valves, hemodynamically significant valve disease, renal failure, or advanced liver disease.

A dose of 20mg a day of rivaroxaban (15mg if CrCl is 15-30 mg/min) reduces the risk of stroke and embolism in non-valvular AF. In the ROCKET trial the rate of stroke/embolism was 2.4%/year for coumadin and 2.1%/year for rivaroxaban. Major bleeding was similar at 3.4% vs.. 3.6% with rates of ICB or fatal bleeding lower but a higher rate of GI bleed with rivaroxaban.

31

1/7/2015

















Apixaban is the only NOAC compared to ASA in AF patients not suitable for coumadin. The study was ended early given apixaban’s superiority. The ARISTOTLE compared coumadin with apixaban in AF with stroke/embolus rate of 1.6% for coumadin and 1.27% for apixaban. The rate of bleeding was similar (3.09%/year vs.. 2.13%/year) but a significantly lower mortality rate and ICB rate with apixaban.

Dabigatran showed greater bleeding than placebo and a numerically lower rate of CAD death, nonfatal AMI, and ischemic stroke it was not statistically significant. With rivaroxaban in TIMI 51 there was a modest reduction in cardiovascular deaths (8.9% vs.. 10.7%) with a reduction in stent thrombosis and significant differences in bleeding. Apixaban in the APPRAISE trial was terminated early for higher rate of major bleeding.

Lab monitoring – none of the NOAC’s require routine lab testing nor is there an available test to quantify the degree of anticoagulation. ◦ PT can show a patient is anticoagulated with apixaban or rivaroxaban but there is no standardization. ◦ Anti-factor Xa assays may be the best means of assessing the anti-FXa NOAC’s but still are not readily available at this time.









Once ACS patients are stabilized on antiplatelets (ASA, clopidogrel) they are considered for anticoagulation depending on the type of stent (DES or BMS). Coumadin plus antiplatelets is not widely accepted but is used. While the NOAC’s are being evaluated for this indication none as of this article’s publication are approved.

Drug interactions – few clinically significant interactions compared to coumadin:

◦ All 3 NOAC’s are substrates for drug transporter Pglycoprotein and can interact with such agents as rifampin. ◦ Rivaroxaban and apixaban are partially metabolized by cytochrome P450 and can interact with strong inducers of that isoenzyme. ◦ The most important clinical issue of renal function as there can be serious bleeding if a patient’s renal function falls or they are used in patients with renal insufficiency/failure.





Dose adjustments – all current NOAC’s are to some degree excreted via the kidney so renal insufficiency does require a reduction in dose. Bleeding events – to date there is no specific reversal agent for the NOAC’s, activated prothrombin complex concentrates have been used with some success but data is limited. ◦ For the most part bleeding is handled with stopping the drug, potential dialysis with dabigatran, and consideration of aPCC’s.

32

1/7/2015



 



NOAC’s are becoming more common for use in VTE, AF prophylaxis long-term, VTE prophylaxis in joint replacement surgery. They offer the advantages over coumadin of less drug-drug or drug-food interactions. They are more bioavailable and consistently achieve therapeutic anticoagulation without the genetic variability seen with coumadin. Bleeding events are less common but exactly how to reverse the NOAC’s is as yet not completely worked out.

Yeah! We are done!

33