LaLonde’s August E-shift

1. Why do we use magnesium sulfate in status asthmaticus?

So Dr. Daouk proposed this question to me (even though I think he already knew the answer…), and I honestly didn’t have a legitimate response. Outside of giving albuterol +/- ipratropium and steroids, the next step is usually ordering 2g of magnesium sulfate. According to multiple studies, this should only be given to patients who have a life threatening exacerbation or whose exacerbation remains severe (peak expiratory flow < 40% of baseline) after one hour of intensive conventional therapy. Of note, the two grams of magnesium should be infused over 20 minutes. Intravenous magnesium sulfate has a bronchodilator effect in acute asthma secondary to the inhibition of calcium influx into airway smooth muscle cells. The routine use of magnesium does not seem to confer significant benefit beyond the conventional use of beta agonists and systemic glucocorticoids. Systematic reviews and meta-analyses have concluded that it is helpful in the subgroup of patients with severe attacks. IV magnesium sulfate has an excellent safety profile, but it is contraindicated in renal insufficiency. There are also some complications from hypermagnesemia including neuromuscular toxicity, bradycardia, hypotension, transient hypocalcemia, and other nonspecific symptoms (nausea, vomiting, flushing).

National Asthma Education and Prevention Program: Expert Panel Report III: Guidelines for the diagnosis and management of asthma. Bethesda, MD. National Heart, Lung, and Blood Institute, 2007. (NIH publication no. 08-4051) http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm (Accessed on September 01, 2007).

Skobeloff EM et al.”Intravenous magnesium sulfate for the treatment of acute asthma in the emergency department.” JAMA. 1989;262(9):1210

 

Alter HJ et al. “Intravenous magnesium as an adjuvant in acute bronchospasm: a meta-analysis.” Ann Emerg Med. 2000;36(3):191

 

2. Age-adjusted D-Dimer for the diagnosis of pulmonary embolism

Before I dive into this topic about our favorite lab, I just want to review some “poor D-dimer candidates.” There are some non-pathological conditions associated with an elevated D-dimer level such as smoking, functional impairment, post operative patients, pregnancy, and race (elevated in African Americans). Some pathologic conditions in which D-dimer is elevated are ACS, GI bleed, aortic dissection, arterial thrombus, atrial fibrillation, DIC, infection, malignancy, pre-eclampsia, sickle cell disease, stroke, superficial thrombophlebitis, and trauma. OK that’s out of the way…

D-dimer measurement is an important step in the diagnostic strategy of clinically suspected acute pulmonary embolism, but its clinical usefulness is limited in elderly patients. An interesting article in JAMA (The ADJUST-PE Study) aimed to validate whether an age-adjusted D-dimer cutoff (age x 10) in patients 50 years or older is associated with an increased diagnostic yield of D-dimer in elderly patients with suspected PE. Their age-adjusted cutoff was derived from studying the effect of a predetermined cutoff (500 mcg/L) on ruling out PE, which was only able to rule out PE in 60% of patients younger than 40 years and only 5% of patients older than 80 years old. They selected patients based on the revised Geneva score or the 2-level Wells Score (found below). Patients who either had high or likely probability of PE proceeded directly to CTA Chest, and with some minor exceptions, everyone else had a D-dimer drawn in order to rule out PE. Of the 3346 total patients (suspected PE included), the prevalence of PE was 19%. Among the 2898 patients with a nonhigh/unlikely clinical probability, 817 patients (28%) had a D-dimer level lower than 500 mcg/L and 337 patients (12%) had a D-dimer between 500 mcg/L and their age-adjusted cutoff. The 3 month failure rate in those 337 patients only yielded 1 missed PE. Hence their conclusion was compared with a fixed D-dimer cutoff of 500 mcg/L, the combination of pretest probability with age-adjusted D-dimer cutoff was associated with a large number of patients in whom PE could be considered ruled out with low likelihood of subsequent clinical venous thromboembolism. Obviously this needs to be studied further, but it’s a fairly large study in a reputable journal and could end up changing clinical practices in years to come.

The Revised Geneva Score
	Points
Age > 65	1
Previous history of PE/DVT	1
Surgery or Fracture within 1 month	1
Active Malignancy	1
Unilateral leg pain	1
Hemoptysis	1
Heart Rate (beats/min)
75-94	1
> 95	2
Pain on calf palpation and unilateral edema	1
Clinical Probability
Low	0 — 1
Intermediate	2 — 4
High	> 5

 

2-Level Wells Score
	Points
Clinical signs and symptoms of DVT	3
Immobilization or surgery in previous 4 weeks	1.5
Heart rate > 100	1.5
Previous history of PE/DVT	1.5
Hemoptysis	1
Malignancy	1
Alternative diagnosis is less likely than PE	3
Clinical Probablity
Unlikely	< 4
Likely	> 4

 

Righini M et al. “Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism: The ADJUST-PE Study.” JAMA. 2014; 311(11):1117-1124.

Jake’s Awesome E-shift

Isolated Vertigo: peripheral etiology vs. posterior stroke (cerebellar infarct) and the use of HINTS

Vertigo is a very common complaint that we deal with daily in the ER. I don’t know about you, but often I feel uncertain how to evaluate patients with the complaint of dizziness. Our job in the ER it to try and identify if the vertigo is the result of a peripheral etiology or central etiology (most concerning for a posterior fossa stroke). Fortunately for us, only 3% of patients that present with vertigo have cerebellar strokes. On top of this, only 10% of those patients diagnosed with stroke lacked other neurologic deficits. Nonetheless, diagnosing a posterior stroke can be a difficult task in the ER, and missing a stroke can be detrimental to both the patient and our careers. Unfortunately, a regular non- contrast CT has poor yield for diagnosing posterior fossa strokes and we are left to determine if the patient needs an MRI of the head with evaluation by a neurologist or if the patient is safe for an out patient evaluation. Last year, Dr Bunting shared an article that looked at using the HINTS criteria to rule out posterior fossa stroke. Today I want to talk about the HINTS criteria and how it can be used to try and rule out or rule in a central etiology for isolated vertigo.

Before we delve deeper into this topic I would like to weed out Benign Positional Paroxysmal Vertigo from persistent vertigo. BPPV is an intermittent vertigo that is often triggered by changing of position, and usually lasting less than one minute following the change in position and is a less worrisome diagnosis than persistent vertigo. The most common cause of BPPV is an otolith in the posterior semicircular canal and can be diagnosed by finding torsional nystagmus on the Dix-Hallpike test. These are the patients that usually require less urgent work up and are usually safe for out patient follow up if the patient has no other signs or symptoms.

Now back to the patient that presents with acute persistent vertigo. First, I want to note that if a patient presents with persistent vertigo and other associated neurologic finds, such as focal neurological deficient, ataxia, speech disturbances, or confusion, you should go down the stroke pathway. However, if the patient presents only with a new complaint of persistent vertigo, we as physicians are required to try and differentiate the cause of this vertigo. As mentioned previously, only 3% of patients that present with new onset persistent vertigo will have a posterior fossa stroke. Therefore, 97% of persistent vertigo can be attributed to peripheral causes such as vestibular neuritis, meniere’s disease, migrainous vertigo or labrinthitis.

So what is HINTS? HINTS is 3 step beside oculomotor exam used to diagnose stroke in patients that present with acute persistent vertigo. HINTS was presented in an article in 2009 by Dr. Newman-Toker. In this article, Newman-Toker presented a prospective, cross-sectional study of 101 high risk patients with acute vestibular syndrome. Of these 101 patients, 76 had stroke and 25 had peripheral etiology based on MRI findings. This study showed that the HINTS exam was 100% sensitive and 96% specific for diagnosing a stroke. The article even went on to say that HINTS criteria may be more sensitive in stroke than an early MRI (that may be stretch).

HINTS – 3 parts Oculomotor exam

1) Head Impulse testing – Have the patient sitting up and focus on your nose. Rapidly rotate the patient’s head sharply to the right and observe and then to the left and observe. In normal exam the eyes will stay stationary and focused on your nose. If the patient has a peripheral etiology for their vertigo, there will be a slight delay in the eyes shifting toward the center to focus on you nose. In patients with a stroke this exam will be normal. With head impulse testing, a normal exam points toward the possibility of a stroke (kind of counterintuitive).

2) Direction changing Nystagmus – Vertigo is often associated with a dominant horizontal nystagmus in one direction. This is not uncommon to see with a vertigo derived from peripheral etiology. The test becomes positive for a central etiology when the patient has a nystagmus that changes direction either horizontally or vertically. In general a vertical nystagmus is a bad thing and a horizontal nystagmus that changes direction is also worrisome. These both would point toward a central cause of vertigo.

3) Test of Skew – The test of skew is looking for vertical ocular misalignment. This misalignment results from a right-left imbalance of vestibular tone. This test is performed by alternating covering each eye. Have the patient look at your nose and cover one eye. Rapidly remove your hand, if there is vertical misalignment, that is abnormal. The patient may also tilt their head to compensate for the misalignment. A positive skew test is most commonly associated with brainstem strokes and has been reported as a herald manifestation of basilar occlusion.

Isolated vertigo with any abnormal HINTS exam requires further neurological evaluation and an MRI to assess for stroke or other central causes. So moving forward how can we incorporate this into our practice. Some may say that the HINTS exam is user dependant and perhaps not safe in the hands of a novice. Well I would suggest that during this time of training, try and perform these three exams on all of your patients with vertigo. Seeing lots of normal will making the abnormal that much more obvious. This will make you that much more comfortable with the exam. Then when you CDU someone that you think could have possibly been discharged, follow up on their MRI. Then perhaps over time we may become more confident in using HINTS to evaluate our patients with vertigo and save some extraneous workups.

Chris Arnold’s July E-shift!

1. What is the optimal outpatient treatment for uncomplicated UTI?

UTI is a common issue faced in the ED, with a broad spectrum of presentation. There are many options for treatment; however, each medication provides advantages and disadvantages. The microbial spectrum of uncomplicated cystitis and pyelonephritis consists mainly of E. Coli 75-95% with Proteus, Klebsiella and Staph. saprophyticus. As the other causes are rare local susceptibility to E. coli should be considered when selecting empirical treatment for UTI.

Treatment of Cystitis

1. Nitrofurantoin 100 mg BID x 5 days
   1. Do not use in early Pyelonephritis as it concentrates in urine
   2. Caution with elderly (cause confusion), and renal disease, CrCL < 60 ineffective
2. Bactrim DS 1 tab BID x 3 days
   1. Do not use if treated for UTI w/ Bactrim in last 3 months
   2. Consider other Abx if local resistance is > 20% (30% at SJH)
3. Fosfomycin 3 g single dose
   1. Less effective than Bactrim and Nitrofurantoin
4. Floroquinolones x 3 days
   1. Not a first line treatment
   2. Local E Coli resistance 34%
   3. Longer treatment regimens did not improve cure rates but did increase side effects.
5. B-lactam agents 3-7 days
   1. Augmentin, cefdinir, cefaclor are all acceptable
   2. Keflex is less well studied but can be used
   3. Amoxicillin and Ampicillin should never be used as they are ineffective.

Treatment of Pyleonephritis

1. Ciprofloxacin 500 mg BID x 7 days
   1. One time IV dose of Cipro shows no added benefit
   2. If reisitance patterns to fluoroquinolones > 10% a long acting IV abx such as Ceftriaxone 1 gram should be given. (34% at SJH)
2. Bactrim DS 1 tab BID x 14 days
   1. Only to be used if pathogen is known to be sensitive to Bactrim
3. Oral B- lactam 10-14 days
   1. Should be given 1 gram Ceftriaxone in ED
   2. Less effective than other options

 

2. If and when is the use of stress dose steroids indicated in the treatment of Sepsis in the ED?

The use of stress dose steroids is a controversial one. Studies have shown overall benefit and a quicker resolution of shock, but no mortality benefit at 28 days. Current guidelines recommend the use of hydrocortisone 100mg q8 for 7 days in patients who require vasopressor support despite adequate fluid replacement. This should also be considered for any critically ill patient taking more than 5 mg of Prednisone for greater than 3 weeks. The rationale behind this is that patients with relative adrenal insufficiency (defined as a post-ACTH cortisol increase <9ug/dl) showed significant shock and mortality reduction in one large multicenter RCT (1).   Further smaller studies have shown significant effects on shock reversal (2-3). Current AAEM guidelines recommend that stress dose steroids be given to any patient requiring vasopressor support (septic shock); they should not be used in patients without evidence of shock. I found some recommendations for increasing the dose by 2-3 fold of daily steroids in patients on a maintenance dose > 5mg of Prednisone with minor infections.

(1) Annane D, Sebille V, Charpentier C, et al: Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 2002;288:862–871

(2) Briegel J, Forst H, Haller M, et al: Stress doses of hydrocortisone reverse hyperdynamic septic shock: A prospective, randomized, double-blind, single-center study. CritCare Med 1999; 27:723–732

(3) Bollaert PE, Charpentier C, Levy B, et al: Reversal of late septic shock with supraphysiologicdoses of hydrocortisone. Crit Care Med 1998; 26:645–650

 

 

3. What is the procedure for and emergent C-section in the ED?

The possibility of being required to perform an emergent C-section in a dead or critically ill mother is one that you might face depending on where you choose to practice. Time is of the essence as a C- section must be preformed within 5 minutes if the baby is to survive. Below is the entire procedure, although some steps will be unnecessary in most instances where we would be performing a C- section.

The book first mentions using 0.5% lidocaine w/ epinephrine to either side of midline from the symphysis pubis to 5 cm above the umbilicus being careful not to pierce the peritoneum or uterus. Ketamine can also be used at a dose of 0.5 mg/kg if analgesia is required for the mother, avoid narcotics or sedatives as they adversely affect the baby. Place patient with R side up to displace uterus to the left

1. Prep patient from below breast to mid thight
2. Enter abdomen through a lower midline incision
3. Identify and incise the peritoneal reflection of bladder transversely and create a bladder flap to retract the bladder
4. Carefully incise the uterus transversely across the lower uterine segment (where the uterine wall thins)
5. Once the amniotic membranes are visible or opened extend the incision laterally bluntly or with bandage scissors careful to advoid the uterine vessels laterally. If necessary extent the incision at one or both of the lateral margins in J fashion with a vertical incision
6. Elevate the fetal part into the incision with an assistant providing fundal pressure
7. Deliver the fetus, suction the nose and mouth, clamp then cut the cord and hand off infant for further care
8. Apply gental traction to the placenta, massage the uterus and begin oxytocin
9. Using gauze sponge clean inside of uterus and vigorously massage fundus to help uterus contract.
10. Close the incision with larger (size 0) absorbable sutures, single layer running is adequate
11. Close the fascia and abdomen once hemostasis is assured.

 

4. What is the treatment for Acute Angle- Closure Glaucoma?

I tend to struggle with eye complaints. I had a patient recently who had acute angle closure glaucoma and wanted to review the treatment. Acute angle closure glaucoma results from sudden increase in IOP from blockage of the anterior chamber outflow channels by the iris root. This causes intraocular vascular insufficiency that may lead to optic nerve or retinal ischemia and can lead to permanent visual loss within hours. It is characterized by sudden onset of blurry vision followed by pain, halos around lights, photophobia, frontal headache and nausea/vomiting.   Exam findings can include red eye with fixed or sluggish mid-dilated pupil, shallow anterior chamber, hazy cornea, and IOP will be greater than 30 mmHg.

Treatment involves reducing the IOP by one or more of the following means.

1. Timolol 0.5% one drop in affected eye
2. Pilocarpine 2% Two drops q15 min for 2-3 hours
3. Mannitol 20% 250-500 ml IV over 2-3 hours
4. Acetazolamide 500 mg PO or 250 mg IV

The patient should also receive an emergent ophthalmologic consultation

Kuper’s July E-shift – Therapeutic hypothermia!

1. What are the measurable benefits of hypothermia after out of hospital arrest?

¹Bernard et al, showed improved outcome (discharge to home/rehab facility versus death or nursing home) in 49% of the 33^o group versus 26% in the normothermia group. This study is a bit disappointing in how it evaluated a ‘good outcome’; some formal neurological and cardiac evaluation of function would have been preferable. Also the power of this study was low (n=77).

Another seminal study² showed which randomized out of hospital arrests to 32^o – 34^o found that positive neurological outcomes were present in 39% of the normothermia group vs 55% in the hypothermia group. Death occurred in 55% of the normothermia group vs 41% in the hypothermia group. Neurological outcomes were based on the Pittsburg cerebral perfusion index (1) no disability, (2) moderate disability, (3) severe disability, (4) persistent vegetative state, (5) death. Good outcomes were considered to be scores of 1 or 2

The evidence for hypothermia was confounded by Niesen et al. 2013, the largest study to date (n=939) randomized people between 33^o and 36^o failed to show a difference in outcome with regard to neurologic function or mortality. This finding lends credence to a growing opinion that the avoidance of hyperexia rather than hypothermia is of the most therapeutic benefit.

2. Who should we include/exclude with regard to out of hospital arrest?

Hypothermia may be considered for comatose adult patients with ROSC from in-hospital or out-of-hospital cardiac arrest with VF arrest showing Class I evidence and asystole or PEA having Class IIB evidence⁵. Survival from time to from collapse >25 min was 3.1% (with no meaningful neurological outcome) versus 65.7% in the <25 min group, while initial presenting rhythm was not an independent variable in one study⁶

 

3. How does delay in initiation of hypothermia affect outcome?

As of 2010 the AHA has not found compelling evidence to recommend a goal time for achieving hypothermia⁵. One large study of 986 failed to show time to initiation as an independent variable for improved outcome⁴. Although animal studies have demonstrated worse outcomes when hypothermia was delayed past 1 hour.

 

4. What are the clinically significant complications of hypothermia?

Pneumonia in hypothermia pts has been reported to be a complication but this was with a small study (n=28). Two other studies failed to show this complication. Increased use in pressors have been noted in hypothermia groups although this finding has not affected mortality. Shivering has been reported in many of the induction phases and because of the increase of metabolic demand Paralytics are recommended. Many electrolyte distrubances have been seen including hypophosphatemia, hypokalemia, hypomagnesemia and hypocalcemia and hyperglycemia, none of which have affected mortality.⁷

 

1. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of- hospital cardiac arrest with induced hypo- thermia. N Engl J Med 2002;346:557-63.

2. The Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346:549-56. [Erratum, N Engl J Med 2002; 346:1756.]

3. Nielsen N, et al for the TTM Trial Investigators. Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest. November 17, 2013 DOI: 10.1056/NEJMoa1310519

4. Sunde K, Pytte M, Jacobsen D, Mangschau A, Jensen LP, Smedsrud C, Draegni T, Steen PA. Implementation of a standardised treatment protocol for post resuscitation care after out-of-hospital cardiac arrest. Resuscitation. 2007;73:29 –39

5. Peberdy, MA et al Post-Cardiac Arrest care: 2010 American Heart association Guidelines for Cardiopulmonary Resuscitation and emergency Cardiovascular Care. Circulation. 2010; 122:S768-S786

6. Oddo, M et al. Early Predictors of Outcome in Comatose Survivors of Ventricular Fibrilation and Non-Ventricular Fibrillation Cardiac Arrest Treated with Hypothermia: A Prospective Study. Crit Care Med. 2008; 36:8

7. Walters, HW et al. The Role of Hypothermia in Post-Cardia Arrest Patients with Return of Spontaneous Circulation: A Systematic Review. Resuscitation. 2011; 82 508-516

Fahad’s July E-shift

1. Does using 2% lidocaine offer any advantage over using 1% lidocaine?

Per Up-to-date, and Roberts and Hedges, higher concentrations of lidocaine beyond 1% do not improve the onset, or the duration of analgesia, and may increase the risk of toxicity. As for toxic doses of lidocaine, they are not to exceed 7mg/kg (0.7 ml/Kg, or maximum of 500mg), when used with epinephrine, and 4mg/kg without epinephrine.

So what are your options if increased onset or duration of analgesia is desired?

One simple approach would be using lidocaine with epinephrine, as that would allow you to use a higher dose of lidocaine without reaching toxic levels. This is particularly advantageous when anesthetizing for laceration repairs in areas that are highly vascular, such as the face. Lidocaine with epinephrine has a more prolonged duration of action when compared to lidocaine alone.

Additionally, other anesthetics such as bupivacaine, mepivacaine, and/or procaine can also be employed, as it has a longer duration of action. This may be more useful in doing nerve blocks to treat dental pain, for example, where the goal is prolonged analgesia until ideally definitive care is sought.

Comparison of commonly infiltrated local anesthetics

Infiltration anesthetic	Concentration (percent)	Physiochemical properties				Maximum allowable dose*		Maximum total dose*
		Lipid:water solubility	Relative potency	Onset of action (min)	Duration (min)	mg/kg	mL/kg	mgequivalent solution volume
Lidocaine
Without epinephrine	1	2.9	2	2-5	50-120	4-5	0.4-0.5	30030 mL of 1 percent
With epinephrine (1:200,000)	1	2.9	2	2-5	60-180	5-7	0.5-0.7	50050 mL of 1 percent
Mepivacaine
Without epinephrine	1	0.8	2	2-5	50-120	5	0.5	30030 mL of 1 percent
With epinephrine•(1:200,000)	1	0.8	2	2-5	60-180	5-7	0.5-0.7	50050 mL of 1 percent
Bupivacaine
Without epinephrine	0.25	27.5	8	5-10	240-480	2	0.8	17570 mL of 0.25 percent
With epinephrine (1:200,000)	0.25	27.5	8	5-10	240-480	3	1.2	22590 mL of 0.25 percent
ProcaineΔ	1	0.6	1	5-10	60-90	7-10	0.7-1	50050 mL of 1 percent

 

2. How should you reverse Coumadin toxicity in a patient with a mechanical heart valve?

The risk of major bleeding has to be weighed against that of valve thrombosis.

If the patient is not bleeding and has an INR of >6, Coumadin can be temporarily discontinued, with small doses of oral vitamin k. With an INR of >10 and no bleeding, higher doses (2-5 mg) of oral vitamin k can be used with close INR monitoring.

If the patient is bleeding, and the bleeding is inaccessible to local control (i.e. intracranial hemorrhage), FFP along with 2.5 to 5 mg of vitamin k should be used. With major bleeding, intravenous unactivated prothrombin complex concentrates (PCC) and low-dose oral or IV vitamin K can be used, with repeated doses of vitamin k at 12 hour intervals. PCC is preferred over fresh frozen plasma, where available.

Recombinant factor 7 is not recommended, as there is insufficient evidence for its efficacy in Coumadin reversal. A study done in the journal Blood in 2010 showed that in healthy subjects showed that while factor 7 reduced the INR, it did not decreased the bleeding in a skin punch biopsy model.

3. Is there a role for urinary amylase in the diagnosis of acute pancreatitis? 

Plasma amylases can enter the urine through glomerular filtration. Conditions that cause increased entry of amylase into plasma (eg, acute pancreatitis) will thus result in increased urinary excretion of amylase. Urinary amylase clearance is increased about 3-fold for 1 to 2 weeks in patients with acute pancreatitis. A value > 550 U/L has been reported as 62% sensitive and 97% specific for acute pancreatitis, while a value > 2000 U/L has been reported as 62% sensitive and 97% specific for acute pancreatitis. Urinary amylase is therefore sometimes used in the diagnosis of acute pancreatitis. However, the rate of urinary amylase excretion appears to be less sensitive than plasma markers, and is not specific for the diagnosis of acute pancreatitis.

Darrius’ review of ST Segment Elevation (it’s not just for MIs!)

ST Segment Elevation Review (9 Cases)

Brugada Syndrome

Cause:  Autosomal dominant inheritance loss of function sodium channelopathy, common in Southeast Asia, men à  associated with life-threatening VT/VF à sudden unexplained nocturnal death

EKG Findings: Characteristic downsloping ST-segment elevation in electrocardiogram leads V1–3 (ST Segment Elevation followed by inverted T wave)

Click here for Brugada EKG Example

Treatment: Admission for iImplantable cardiac defibrillator (ICD)

 

Hyperkalemia

Cause:  Adrenal Insufficiency, End Stage Renal Disease, Rhabdomyolysis, Tumor Lysis Syndrome, Digoxin Toxicity, etc., Usually seen with K values 5.5-7.5 mEq/L

EKG Findings:  Peaked T waves (K 5.5-7.5), ST Segment Depression (K 7.5-10), Bundle Branch Block (K>10 mEq/L).

Click here for Hyperkalemia EKGs

Treatment: Calcium Gluconate, Albuterol nebulized, Insulin/glucose, Sodium polystyrene sulfonate, Sodium Bicarbonate, Furosemide, Hemodialysis

 

Hypothermia

Cause: Core temperature < 35 C (< 95 F), hypothermia caused by heat loss via conduction (direct contact), radiation (no insulation), evaporation of water, convection (wind) losses.

EKG Findings: Osborne (or J wave) Wave –  a slow, positive deflection at the end of the QRS complex

Click here for Hypothermia EKG

Treatment: Remove patient from cold environment, re-warm (passive, active such as warm water immersion, active core rewarming (such as GI lavage and or pleural lavage).

 

Left Bundle Branch Block

Cause: A block in infranodal conduction from the AV node.  Differential inferior MI, hyperkalemia, cardiomyopathy, valvular, myocarditis, cardiac surgery, congenital heart conditions, degenerative processes (Lev’s Disease)

EKG Findings:  Complete LBBB – Prolonged QRS, Broad Monophasic R wave leads I and V6,

Complete LBBB suggestive of Acute Myocardial Infarction – > 1mm ST elevation concordant with QRS, > 1 mm ST depression in leads V1-V3, > 5mm ST elevation discordant with QRS

Click here for LBBB EKGs

Treatment:  Complete LBBB suggestive of acute myocardial infarction – percutaneous coronary intervention / fibrinolytics / cardiology consultation immediate

 

Left Ventricular Aneurysm

Cause: Occurs 5-14 days post MI in 1-4.5% of AMI patients

EKG Findings: Persistent ST segment elevation following an AMI (> 2 weeks)

Click here for LV Aneurysm EKG

Treatment: Cardiac Surgery

Myocardial Infarction

Cause:

• Myocardial infarction results when arterial blood flow to the myocardium is suddenly decreased
• Usually due to atherosclerotic coronary artery disease with plaque rupture and sudden occlusion by thrombus; vasculitis or emboli less common
• Complete occlusion, most often with thrombus, is found in 80–90% of patients with chest pain and ST segment elevation
• Cocaine associated with coronary artery spasm

EKG Findings:

50% of patients: hyperacute T waves à flipped T- waves à elevated ST segments à ST segment elevation myocardial infarction àQ waves half of patients

Other half nonspecific ST or T wave changes, or may be normal

STEMI EKG

Treatment:

2 methods available

• pharmacologic thrombolysis via plasminogen activators
• percutaneous coronary intervention (PCI)
• effectiveness of depends on how early it is given after symptom onset

Immediate Measures

• cardiac monitor, given oxygen, 2 peripheral IV’s placed
• Aspirin 162-325 mg – first and most important medication given to ACS patients
• If Aspirin contraindicated, use 300 mg clopidogrel
• 12 lead ECG within 10 minutes of arrival
• If chest pain is present, give nitroglycerin, 0.4 mg sublingually Repeat if no effect occurs in 5 minutes. If chest pain returns or continues and systolic blood pressure is above 100 mm Hg, start intravenous nitroglycerin at 10 μg/min and increase by 5 μg/min every 3–5 minutes until systolic blood pressure falls by 10% or chest pain is relieved
• Morphine may be still be used for analgesia, particularly for STEMI patients. However for UA/NSTEMI patients it may have increased adverse effects

 

Pericarditis

Cause: Idiopathic, Infectious (Cocksackie Virus), Malignancy, Drug induced (hydralazine), Radiation, Post-MI, Uremia, Rheumatological disease

EKG Findings:  Diffuse ST Segment Elevation, ST segment returns to isoelectric line, PR Depression

Click here for Pericarditis EKG

Treatment: NSAIDS, consider further work-up underlying cause

Pulmonary Embolism

Causes: Hypercoagulable state, nephritic syndrome, DIC, oral contraceptives, Lupus, Malignancy

EKG Findings: S1Q3T3 (seen 15%), ST-T wave changes

Click here for PE EKG

Treatment:  Anti-coagulants, IVC filter, fibrinolytics (unstable), Surgical embolectomy

 

Early Repolarization

Cause:  Normal electrical variant – seen in healthy young males, athletes

EKG Findings:  Concave ST segment elevation of 1 to 3 mm in precordial leads, No reciprocal ST segment depression

Click here for Early Repolarization EKG

Treatment:  None