Acute-Onset Atrial Fibrillation: “Answers”

1. What is your approach to managing a patient with acute-onset (< 48 hours) atrial fibrillation (afib)?  Which patients do you cardiovert? Does your management algorithm differ for patients with acute-onset rapid afib?

The management of acute-onset afib in stable patients remains controversial. (Clearly, in those that are unstable, immediate electrocardioversion is indicated). Historically, many of these patients have been managed with rate control and anticoagulation as necessary. This approach seemed supported by the RACE and AFFIRM trials, which found rate control to be non-inferior and/or preferable to rhythm control. However, these studies were performed in outpatients with chronic atrial fibrillation. These patients were, on average, older and with established cardiac disease, thus there is much debate about whether the results can be extrapolated to apply to those with acute-onset afib, especially in the ED.

A growing body of research on acute-onset afib is beginning to suggest that ED cardioversion may be safe and effective, and that it could decrease admission rates and ED length of stay. It may also reduce the need for outpatient medication such as anticoagulation and rate-controlling meds. A few studies evaluating one- and six-month outcomes have not shown an increase in thromboembolic events in those who were cardioverted in the ED. The longer a patient remains in afib, the less likely it will be that a later cardioversion attempt will be successful. Therefore, ED cardioversion may give the patient a better chance of returning to a sinus rhythm (Fuster, 2011).  The approach of cardioverting acute-onset afib, has been protocolized by a research group in Canada as the Ottawa Aggressive Protocol, and is increasingly being used there.

The key element in determining which patients to cardiovert is duration of the arrhythmia. Time since onset must be clear and less than 48 hours.  Additional factors may include severity of symptoms (with more severe symptoms pushing the balance towards cardioversion), and patient history (i.e. if a patient has a history of paroxysmal afib and has been successfully cardioverted in the past).

Whether the presenting rhythm is rate-controlled or not should not influence the decision of whether to cardiovert. The only proviso is that patients with RVR are more likely to be hemodynamically unstable and/or symptomatic, which may make the cardioversion (or at least rate control) more urgent. As rate control can be more quickly accomplished than setting up for electrocardioversion, it is reasonable to administer rate-controlling medications in a symptomatic patient, and then proceed with cardioversion.

The management of acute-onset afib, of course, warrants an investigation into potential causes of the arrhythmia.

2. If you decide to cardiovert a patient, do you prefer to use chemical or electrical cardioversion? Do you take a sequenced approach? Which agents do you prefer for chemical cardioversion?

Again, there is no agreed upon approach to cardioversion. Some advocate going directly to electrocardioversion, as it has a higher success rate (80-95%) over chemical cardioversion alone (50-70%), is faster, and lacks the pro-arrhythmic potential and possible side effects of anti-arrhythmic agents (Decker, 2011). Others recommend taking a sequenced approach of an attempted chemical cardioversion followed by electrocardioversion if the former fails. There are some data to suggest that giving an anti-arrhythmic agent before attempting electrocardioversion may increase the success of the electrocardioversion; however, most of these studies were performed with patients in chronic afib. At this time, the ACC/AHA considers pretreatment with anti-arrhythmics before cardioversion in acute-onset afib to be optional (Fuster, 2011).  If cardioversion is the goal, it is our opinion that electrocardioversion should be attempted first as it is faster and more effective. If this fails, the patient can be rate-controlled and then admitted for either attempted chemical cardioversion or establishment of long-term rate-control/anti-coagulation management.

Several agents have been used to attempt chemical cardioversion. These include flecainide, propafenone, ibutilide, dofetilide, amiodarone, procainamide, and others, with the first four listed as Class I recommendations by the ACC/AHA (Fuster, 2011). The decision of which to use will depend in large part on patient symptoms, presence of underlying heart disease, presence of QT interval abnormalities, and whether the drug will require telemetry due to pro-arrhythmic potential. While procainamide is not regularly used by cardiologists, the group advocating the Ottawa Agressive Protocol have argued it is effective and safe to use in the ED with subsequent discharge of patients. Although it has not been tested sufficiently in chronic atrial fibrillation to make it a recommended drug by the ACC/AHA, it has been used amply in acute-onset afib, with several studies suggesting its superiority to placebo (Fuster, 2011).

It is interesting to note that amiodarone is considered a Class IIa recommendation by the ACC/AHA. Even though its success rate in cardioverting atrial fibrillation patients over 24 hours is quite good, it has a low cardioversion rate within 8 hours of administration, making it a less useful medication in the ED (Chevalier, 2003). Looking to the future, a new antiarrhythmic drug, vernakalant has shown great promise in achieving sinus rhythm in acute-onset atrial fibrillation. It has been approved in Europe but is still pending FDA approval.

3. Which patients do you choose to anticoagulate? What approach do you take to anticoagulation?

The question of anticoagulation applies to both BEFORE and AFTER conversion. For patients who have been in afib for less than 48 hours, anticoagulation need not be started before cardioversion.  If, however, the patient has been in afib for either an unknown amount of time or more than 48 hrs, he or she will either need a TEE to evaluate for the presence of an atrial thrombus or be anticoagulated for 3 weeks before cardioversion. After successful cardioversion, the patient would typically be placed on 4 weeks of anticoagulation.

Regarding anticoagulation after conversion of an acute-onset afib, approaches vary. It is worth noting that risk of stroke is 5-15 times higher without anticoagulation in afib (both chronic and paroxysmal). Thus, if the patient has had prior episodes of acute-onset afib (i.e., PAF), then the patient should probably be anticoagulated based on his/her CHADS-2 score.  If, however, this is the first known episode of atrial fibrillation and sinus rhythm is achieved, it is not necessary to start the patient on anticoagulation.  In the Ottawa Aggressive Protocol, none of the patients were started on anticoagulation after successful conversion, regardless of whether the afib was paroxysmal or new.

 
4: Which patients with acute-onset afib do you admit and which do you discharge?  If the patient is successfully cardioverted, do you admit or discharge?  If you discharge them, do you prescribe them any anti-arrhythmic agents?

If a patient with new onset afib is successfully electrocardioverted, shows no signs of cardiac ischemia, and is asymptomatic, he or she can safely be discharged after a short period of cardiac monitoring to ensure continued sinus rhythm.  If a patient has been chemically cardioverted, a longer ED stay, or possibly a telemetry admission, may be warranted, depending on the pro-arrhythmic potential of the agent used. As noted above, in at least one Canadian study, procainamide was used with subsequent ED discharge of patients successfully cardioverted.

If the patient fails the above criteria he or she should be admitted. If cardioversion is attempted and failed, the patient should be rate-controlled and admitted. If no cardioversion is attempted, the patient should be rate-controlled, but whether to admit them depends on the patient’s age, symptoms, comorbidities, access to quick cardiology follow-up, success of rate control in the ED, and comfort of the practitioner with starting outpatient anticoagulation as needed. Ultimately, many of these patients are admitted.

For patients successfully cardioverted in the ED who are set to be discharged, it is not necessary to start them on an anti-arrhythmic. Data suggest that while anti-arrhythmics do reduce (but far from eliminate) recurrence of atrial fibrillation, they have multiple adverse effects associated with them, including being pro-arrhythmic and in the case of some, increasing mortality rates (Lafuente-Lafuente, 2007). Amiodarone has been shown to be among the more effective agents, but of course has serious side effects and is therefore not recommended for long-term use. Bottom line: let your patient’s cardiologist sort this out as an outpatient. Do not start them in the ED (indeed, doing so would likely necessitate an admission to monitor for arrhythmias).

Of course, any patient presenting with recent-onset afib who is discharged should have close cardiology follow-up, even if successfully converted, as recurrence rates of afib are high (71-84% at one year), and because they will need a more thorough cardiac evaluation including a TTE, etc.

References and Further Reading

Chevalier P, et al. Amiodarone versus placebo and class Ic drugs for cardioversion of recent-onset atrial fibrillation: a meta-analysis. J Am Coll Cardiol. 2003; 41: 255– 62.

Decker WW, et al. A prospective, randomized trial of an emergency department observation unit for acute onset atrial fibrillation. Ann Emerg Med. 2008 Oct; 52(4): 322-8.

Decker WW and Stead LG. Selecting rate control for recent-onset atrial fibrillation. Ann Emerg Med. 2001 Jan; 57(1): 32-3.

Fuster V, et al. 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 Guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in partnership with the European Society of Cardiology and in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. J Am Coll Cardiol. 2011 Mar 15;57(11):e101-98.

Lafuente-Lafuente C, et al. Antiarrhytmics for maintaining sinus rhythm after cardioversion of atrial fibrillation. Cochrane Database Syst Rev. 2007 Oct 17;(4).

Michael JA, et al. Cardioversion of paroxysmal atrial fibrillation in the emergency department. Ann Emerg Med. 1999 Apr; 33(4): 379-87.

Scheuermeyer XF, et al. Thirty-day outcomes of emergency department patients undergoing electrical cardioversion for atrial flutter or fibrillation. Acad Emerg Med. 2010 Apr; 17(4): 408-15.

Stiell IG, et al. Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. CJEM. 2010 May; 12(3): 181-91.

Van Gelder IC, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med. 2002 Dec 5; 347(23): 1834-40.

Wyse DG, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med. 2002 Dec 5; 347(23): 1825-33.

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August 2011: Acute Coronary Syndrome, Questions

1. What anti-coagulants and/or anti-platelet agents do you use in a patient with a STEMI?  In an NSTEMI?

2.  How do you identify and manage patients with unstable angina?

3.  How do you risk stratify patients with chest pain?  Do you use any clinical decision rules?

4.  How reassuring is a recent (< 1 year) negative stress test in managing a patient with chest pain? How about a recent “normal” cath (i.e., < 30% blockage, no intervention)?

ACS Questions Poster

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Acute-Onset Atrial Fibrillation: Questions

1. What is your approach to managing a patient with new-onset (e.g., within the last 24 hours) atrial fibrillation?  Which patients do you cardiovert? Does your management algorithm differ for patients with new-onset atrial fibrillation with rapid ventricular rate (RVR)?

2. If you decide to cardiovert a patient, do you prefer to use chemical or electrical cardioversion? Do you take a sequenced approach? Which agents do you prefer for chemical cardioversion?

3. Which patients do you choose to anticoagulate? What approach do you take to anticoagulation?

4: Which patients with new onset afib do you admit and which do you discharge?  If the patient is successfully cardioverted, do you admit or discharge?  If you discharge them, do you prescribe them any anti-arrhythmic agents?

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Mammal Bites: “Answers”

1.  Which mammal bites get antibiotics?  Cat versus human versus dog?  Location of the bite?

From a Cochrane review of the topic, which looked at all known randomized controlled trials (RCTs) on the subject:

“The use of prophylactic antibiotics was associated with a statistically significant reduction in the rate of infection after bites by humans. Prophylactic antibiotics did not appear to reduce the rate of infection after bites by cats or dogs. Wound type, e.g. laceration or puncture, did not appear to influence the effectiveness of the prophylactic antibiotic. Prophylactic antibiotics were associated with a statistically significant reduction in the rate of infection in hand bites (OR 0.10, 95% CI 0.01 to 0.86; NNT = 4, 95% CI 2 to 50).”

2.  Which mammal bites do you close primarily and which do you leave open?  What’s your time window? Does it vary by mammal or location?

This is an area of controversy. A number of studies (including Chen, et al), have found that properly inspected, debrided, and irrigated wounds can be closed on most areas of the body with a 6-7% infection rate.  Hand wounds, cat bites, and human bites are associated with higher rates of infection, and therefore much more caution is warranted.  In terms of time window and type of closure, a rough consensus (open to much debate) is as follows:

Primary closure: head/face/neck/torso/proximal extremities (typically not hands and feet) lacerations, that occurred 12 hours or less from the time of presentation

Delayed primary closure: face and non-extremity wounds greater than 12 hours, or showing signs of infection. Typically, wound care is continued (debridement, antibiotics, etc.) for 72 hours, then the wound is re-evaluated for closure

No closure: Continuing infection, crush or puncture wounds, bites to the hands and feet, and clenched-fist injuries (fight bites)

3.  How do you irrigate bite wounds?  Do you use betadine?

Copiously.  You need about 7psi to irrigate most wounds. A 19-gauge or larger catheter with a 35-mL syringe is sufficient, as are most pedal sinks at full blast.  Most experts recommend 100-200mL of water per square inch for most wounds (i.e., not grossly contaminated).

According to Trott’s Wounds and Lacerations: Emergency Care and Closure, Betadine is one of the most potent bactericidal agents used in wound care. It is active against gram negatives, gram positives, fungi, and viruses. Betadine (povidone-iodine) comes as a 10% solution. It can be safely used to irrigate wounds only when diluted to a 1% concentration (i.e., a ten-fold dilution) or lower, as is evidenced by the ophthalmology literature.

4.  Which patients with bites do you admit?

Clearly, those going to the OR, or requiring IV antibiotics. We often admit the majority of our fight bites, in part because of patient reliability, and because of the high incidence of infection. The party line is:  consider admission in suspected tendon/joint/cartilage involvement; systemic infection; and in those unlikely to follow up.

References and Further Reading

Abrahamian FM, et al. Management of skin and soft tissue infections in the emergency department. Infect Dis Clin North Am. 2008; 22(1): 89-116.

Chen E, et al. Primary closure of mammalian bites. Acad Emerg Med. 2000; 7(2): 157-161.

Medeiros I and Saconato H. Antibiotic prophylaxis for mammalian bites. Cochrane Database Syst Rev. 2001; 2: CD001738.

Trott AT. Wounds and lacerations: emergency care and closure. Third edition. Mosby. 2005.

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Mammal Bites: Questions

1. Which mammal bites get antibiotics?  Cat versus human versus dog? Location of the bite?

2. Which mammal bites do you close primarily and which do you leave open?  What’s your time window?  Does it vary by mammal or location?

3. How do you irrigate bite wounds?  Do you use betadine?

4. Which patients with bites do you admit?


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Rapid Sequence Intubation, Episode 1: “Answers”

1. What is RSI, and why do we use it for most ED intubations?

“Rapid Sequence Intubation (RSI) is the administration, after preoxygenation, of a potent induction agent followed immediately by a rapidly acting neuromuscular blocking agent to induce unconsciousness and motor paralysis for tracheal intubation” (Walls and Luten).

We use RSI in the ED for a number of reasons.  Unlike in the OR, we don’t get time for a full pre-operative evaluation of patients, pre-op clearance by a patient’s primary care physician, etc. In addition, patients are usually unstable/critically ill and need immediate, emergent airway protection via intubation.  RSI is the fastest and safest way, under most circumstances, of obtaining this airway protection.

Numerous studies have shown that paralysis with induction optimizes intubation conditions in the ED and our success rate with this modality is extremely high (> 95% in medical patients and > 90% in trauma/surgical patients) (Walls and Luten).  Paralytics are particularly useful because they help in the prevention of gastric content aspiration.

2. What are the “Seven P’s” of RSI?

The  “Seven P’s” are the key steps in RSI.  They are:

Preparation

Preoxygenation

Pretreatment

Paralysis and Induction

Positioning

Placement with proof

Postintubation management

Please note that “panic” is not one of the Seven P’s.

3. Atropine, Fentanyl and lidocaine are some of the typical agents used in the pretreatment phase of RSI. When and why do you use any of these drugs?

Atropine: This drug is most commonly used in pediatric patients (particularly < 2 years of age) to attenuate reflex bradycardia associated with succinycholine administration in RSI.  The idea is that kids tolerate tachycardia very well but do poorly with bradycardia.  The dose of atropine for pretreatment is 0.01 mg/kg IV (minimum dose is 0.1 mg). Although it continues to be recommended by a number of professional societies, randomized control trials have shown no difference in the rate of clinically significant bradycardia in pediatric patients receiving succinycholine whether they got atropine or not (McAuliffe, et al). Most airway “gurus” have dropped atropine as a recommendation for pretreatment but suggest having it at the bedside if bradycardia occurs, especially in patients under the age of one.

Fentanyl: Fentanyl pretreatment is thought to attenuate the sympathetic response to direct laryngoscopy.  This sympathetic response can drive up heart rate, blood pressure, and ICP and so may be detrimental to patients, especially those patients with ischemic heart disease, aortic dissections, intracranial hemorrhage, etc.  The dose required for full attenuation is 11 – 15 mcg/kg but this large a dose may cause significant hypotension.  Doses as low as 2-3 mcg/kg will produce some attenuation and are more reasonable for RSI purposes. Important to note is that the use of opioids in pretreatment for head trauma is an area of controversy.  The Walls text recommends it, but be aware there is some evidence to suggest that it may increase ICP in patients with head injury (de Nadal, et al).

Lidocaine: Lidocaine pretreatment is also believed to dampen the response to direct laryngoscopy, but instead of affecting the entirety of the sympathetic response, lidocaine may attenuate the bronchoconstriction and increased intracranial pressure caused, of use in patients intubated for asthma or elevated ICP (due to bleed, trauma, mass, etc.) (Lev and Rosen).  A Cochrane review update of a 2001 article by Robinson and Clancy found no evidence that pretreatment with lidocaine in patients with head injury undergoing RSI improved neurological outcomes.  The dose for  increased ICP and reactive airway disease is 1.5 mg/kg IV.

Remember that pretreatment must be given at least 3-5 minutes prior to induction and paralysis.  Pretreatment should never delay intubation in a patient with hypoxia.

4. What is the role for defasciculating doses of paralytic agents?

In the past, defasciculating doses of succinycholine, or pretreatment with a non-depolarizing agent prior to succinycholine, was recommended to prevent fasciculations.  The idea was that fasciculations cause increased intracranial pressure and were thus detrimental to patients with head trauma.  While some studies have suggested that fasciculations associated with succinycholine increase ICP, there has never been any evidence to show that it leads to changes in morbidity or mortality.  In addition, more recent studies have called into question whether fasciculations increase ICP at all (Clancy, et al, 2001).

References and Further Reading

Clancy M, et al. In patients with heady injuries who undergo rapid sequence intubation using succinylcholine, does pretreatment with a competitive neuromuscular blocking agent improve outcome?  A literature review. Emerg Med J. 2001; 18(5): 373-375.

de Nadal M, et al. Effects on intracranial pressure of fentanyl in severe head injured patients. Acta Neurochir Suppl. 1998; 71: 10-12.

Fastle RK and Roback MG. Pediatric rapid sequence intubation: incidence of reflex bradycardia and effects of pretreatment with atropine. Pediatr Emerg Care. 2004; 20(10): 651-655.

Lev R and Rosen P. Prophylactic lidocaine use preintubation: a review. J Emerg Med. 1994; 12(4): 499-506.

Robinson N and Clancy M. In patients with head injury undergoing rapid sequence intubation, does pretreatment with intravenous lignocaine/lidocaine lead to an improved neurological outcome? A review of the literature. Emerg Med J. 2001; 18 (6): 453-457.

Walls RM. Lidocaine and rapid sequence intubation. Ann Emerg Med. 1996. 27(4): 528-529.

Walls RM and Luten RC. Manual of Emergency Airway Management. Third Edition. Lippincott. 2008.

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Rapid Sequence Intubation, Episode 1: Questions

1. What is RSI, and why do we use it for most ED intubations? 

2. What are the “Seven P’s” of RSI?

3. Atropine, fentanyl, and lidocaine are some of the typical agents used in the pretreatment phase of RSI.  When and why do you use any of these drugs?

 

4. What is the role for defasciculating doses of paralytic agents in RSI?

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Acute Pulmonary Edema: “Answers”

Updated May 2014

1. What is the basic pathophysiology of APE? How does this differ from a CHF exacerbation?

Acute pulmonary edema (APE) or Acute decompensated heart failure (ADHF) results from a host of mechanisms. Historically, it was believed that edema resulted from decreased blood flow to the kidneys and decreased kidney function. This cardiorenal model from the 1940s led to the broad use of loop diuretics for treatment. In the 1970s, this model was replaced by the cardiocirculatory model based on invasive monitoring studies showing increased peripheral vascular resistance. This model stated that the increased vascular tone led to increased preload and afterload straining the left ventricle leading to failure. Finally, in the 1990s, the neurohormonal model emerged. It became well understood at this time that numerous neurohormonal mediators including dopamine, norepinephrine, adrenaline and angiotensin affected cardiac function and vascular tone. The sympathetic surge from these hormones and activation of the renin-angiotensin-aldosterone system (RAAS) leads to vasoconstriction, tachycardia and worsening cardiac function.

APE answersCongestive heart failure (CHF) exacerbations differ from APE mainly in terms of the severity of neurohormonal activation. In particular, patients with CHF exacerbations are not typically sympathetically stimulated to the same degree (i.e., they do not exhibit marked tachypnea, tachycardia, hypertension, and sweating).

As afterload increases, the left ventricle (LV) is unable to adequately handle pulmonary venous return leading to alveolar congestion. Pulmonary capillaries experience increased hydrostatic pressure leading to leakage of fluid into the alveolar space. Additionally, leakage of fluid into the alveolar space washes away pulmonary surfactant.

While it is clear that there is increased fluid in the cardiopulmonary system, the origin of the fluid has been hotly debated for decades. The cardiorenal model preaches that increased circulating volume results from fluid retention due to decreased kidney function. However, Zile demonstrated that patients presenting in APE had increased cardiac filling pressure without significant change from their dry weight(Zile, 2008). Chaudry and colleagues quantified this finding that 50% of patients in APE had < 2 lbs of weight gain (Chaudry, 2007). Instead of fluid gain, it is more likely that the increased cardiac filling pressures are due to fluid shifts, specifically, constriction within the splanchnic circulation (Fallick, 2011).

With the elucidation of the neurohormonal mechanisms leading to APE, treatment should be targeted at interrupting these processes.

2. What medications do you use for immediate management of APE and why?

Patients who present with APE are typically markedly hypertensive and in acute respiratory distress. Rapid initiation of appropriate treatment is vital to reversing the neurohormonal surge and rescuing patients from respiratory and complete cardiac failure. Immediate interventions should focus on reduction of afterload and preload as well as respiratory support.

Nitroglycerin (NTG) is the most important first-line medication in treatment. NTG at lower doses acts as a venodilator leading to decreased preload and at higher doses (> 100 mcg/min) is a potent afterload reducer. It can be given sublingually, transdermally and intravenously making it easy to administer and easy to titrate. Studies have looked at the use of nitroglycerin in APE (Bussmann, 1978), compared it to loop diuretics (Cotter, 1998) and investigated the application of high-doses (Levy, 2007).

The key is to start the patient early on nitroglycerin and rapidly titrate up. A sublingual tab of 400 mcg is the approximate equivalent of 40-60 mcg/min for 4-5 minutes. If the patient tolerates this dose, it is reasonable to start the IV infusion at 50 mcg and rapidly titrate up. Often, doses of upward of 200 mcg/min are required to effectively reduce preload. Once the 100 mcg/min threshold is achieved, the patient will also experience the benefits of afterload reduction.

Angiotensin converting enzyme inhibitors (ACEI) are less studied but have been recommended in patients with APE as they are potent afterload reducers. ACEI act by halting the RAAS activation described above. Hamilton performed an RDCT of sublingual captopril in addition to standard therapy versus standard therapy alone and found that the addition of an ACEI led to increased patient comfort and a non-significant decrease in respiratory failure (Hamilton 1996). Another small study showed improved cardiac index and stroke volume resulting from ACEI use (Haude 1990). Sacchetti, et al. showed that ACEI use in APE patients was associated with a lower ICU admission rate (OR = 0.29) and lower intubation rates (OR = 0.16) (Sacchetti 1999).

Morphine and loop diuretics represent two previously recommended interventions that have been found to be less helpful and potentially harmful. Morphine, long a part of the APE algorithim, is not effective in afterload reduction and has been shown in observational and retrospective studies to increase morbidity and mortality (Hoffman, 1987; Sacchetti, 1993; Sacchetti, 1999; Peacock, 2008). It should no longer be part of our treatment package.

Loop diuretics should also not be used early in treatment. As discussed earlier, 50% of patients do not have significant volume overload. Increased cardiac filling pressure results from shifts in fluid instead of fluid retention. Additionally, many of the patients who are volume overloaded have ESRD and loop diuretics will not be useful. Finally, small studies have shown an initial increase in preload resulting from loop diuretic administration, potentially leading to worse outcomes (Kraus 1990). Felker and colleagues give a passionate argument on the low utility of loop diuretics (Felker 2009).

3. What is the role of NIPPV in APE? Which is preferred: CPAP or BiPAP?

Non-invasive positive pressure ventilation (NIPPV) can be applied either via continuous positive airway pressure (CPAP), or bilevel positive airway pressure (BiPAP). Both are effective at decreasing the work of breathing. APE patients have decreased lung compliance because they have washed away their surfactant and have atelectatic lungs and/or alveolar collapse. The “threshold work,” the energy necessary to open these alveoli, is dramatically higher in APE (over 25% consumption of energy compared to less than 3-4% in the normal lungs). CPAP and BiPAP reduce the work of breathing by “stenting” the alveoli open during expiration and thus diminishing the energy consumption needed to open the alveoli during each inspiration. The resultant decrease in work of breathing allows for a greater amount of energy to be devoted to cardiac work and thus potentially increases LV function

Simultaneous to the initiation of NTG therapy, non-invasive positive pressure ventilation (NIPPV) should be started. There are a host of articles demonstrating that NIPPV decreases intubation rates and ICU utilization by improving respiratory function (Mehta, 1997; Nava, 2003; Gray, 2008). A very recent study found a reduction in ICU admissions from 92 to 38% with the use of bilevel NIPPV (Liesching 2014).

4. When do you intubate?

As with all critical disease processes, the decision to intubate is a clinical one. There are no guidelines, lab values or vital signs that can give you this answer. In general, these patients are older and have less cardio-pulmonary reserve and, as a result, tend to tire quickly.

Failure to oxygenate or ventilate, evidence of tiring, and failure to tolerate NIPPV are just some of the criteria used to consider intubation. It is important to note that intubation and mechanical ventilation will allow the patient to decrease their work of breathing and increase the available energy for myocardial demand, which may improve cardiac function.

Related Resources

Furosemide in the Treatment of Acute Pulmonary Edema from the emDocs BlogEMCRit Podcast 1 – Sympathetic Crashing Acute Pulmonary Edema

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Acute Pulmonary Edema: Questions

1. What is the basic pathophysiology of acute pulmonary edema (APE)?  How does this differ from a CHF exacerbation?

2. What medications do you use for immediate management of APE and why?

3. What is the role of non-invasive positive pressure ventilation (NIPPV) in APE?  Which is preferred: CPAP or BiPAP?

4. When do you intubate?

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Pelvic Inflammatory Disease “Answers”

1. Which factors on history and physical make you think a patient has more than cervicitis?

Greater than 90% of patients with PID present with bilateral, lower abdominal pain. Time of onset is similarly suggestive, with up to 75% of cases beginning in the first week after the onset of menstruation. While neither sensitive nor specific, 75% of PID patients will have new discharge, and half will have a fever. Obviously the presentation can vary, including manifold symptoms such as dysuria, vomiting, and back pain. The only physical findings that are routinely found (in > 90% of laparoscopically verified PID) are lower abdominal tenderness, adnexal tenderness, and cervical motion tenderness.  No lab test is consistently useful in diagnosing PID (apart from a verified diagnosis of GC or CT), including CBC (only around 60% of PID patients have a WBC > 10,000).  There is some data to suggest transvaginal ultrasound may aid diagnosis, but this is still an area of controversy. Bottom line: The criteria for diagnosis of PID are very subjective.  Because of the important consequences of untreated PID (TOA, infertility), you should have a very low threshold to treat a woman with cervicitis as PID.

2. Which antibiotic regimen do you use to treat patients with PID?  Do you routinely include metronidazole in your regimen?

The most common outpatient regimen is doxycycline for fourteen days plus ceftriaxone or cefoxitin IM once.  Inpatient regimens are most typically doxyccyline (IV/PO) plus an appropriate cephalosporin (ceftriaxone) or cephamycin (cefoxitin). Clindamycin and gentamicin are another inpatient option. Note that outpatient regimens for patients truly allergic to cephalosporins are limited. In terms of metronidazole, clearly those with concomitant bacterial vaginosis or trichomonas should receive it, but the CDC also recommends including it when there is a pelvic abscess (see question #3) and in anyone with a history of gynecologic instrumentation in the prior month.

3. What imaging do you order? When do you image?

PID does not require any imaging for diagnosis or management.  However, the complications associated with PID, notably tubo-ovarian abscess (TOA), require imaging for diagnosis. For years, the standard teaching had been that ultrasound was the diagnostic modality of choice for the diagnosis of TOA.  Retrospective studies noted sensitivities as high as 93% in the past.  These studies basically looked at the rate of positive ultrasounds in patients with PID and a palpable adnexal mass.  Unfortunately, this only represents a small subset of TOA patients. More recent literature has challenged these findings and suggests a more modest sensitivity, near 83%.  The only prospective trial with a gold standard (laparoscopy) found that MRI had a sensitivity approaching 100% and a specificity of around 90%.  Preliminary studies on CT scanning with IV contrast suggest a sensitivity in the mid to high 90% range but there is inadequate data at this time to definitively state the utility of CT in this diagnosis.

4. Which patients do you admit?

Currently, only 15-25% of women diagnosed with PID are hospitalized. The CDC guidelines recommend it when: (1) the diagnosis is uncertain, (2) the possibility of surgical emergencies such as appendicitis and ectopic pregnancy cannot be excluded, (3) a pelvic abscess is suspected, (4) the patient is pregnant, (5) the patient is an adolescent, (6) severe illness precludes outpatient management, (7) the patient is unable to follow or tolerate an outpatient regimen, (8) the patient has not responded to outpatient therapy, or (9) clinical follow-up cannot be arranged within 72 hours of the initiation of antibiotic treatment.

References and Further Reading:

Eschenbach DA. Acute pelvic inflammatory disease: Etiology, risk factors, and pathogenesis. Clin Obstet Gynecol 1976; 19: 147.

Korn AP, et al. Risk factors for plasma cell endometritis among women with cervical Neisseria gonorrhoeae, cervical Chlamydia trachomatis, or bacterial vaginosis. Am J Obstet Gynecol. 1998; 178: 987.

Lambert MJ, Vila M. Gynecologic ultrasound in emergency medicine. Emergency medicine clinics of North America. 2004; 22.

McCormack WM. Pelvic inflammatory disease. N Engl J Med. Jan 13 1994;330(2):115-9.

“Pelvic Inflammatory Disease.” Centers for Disease Control. Sexually Transmitted Diseases Treatment Guidelines 2010.

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