EKG of the Week 2017 5-14

This EKG comes courtesy of Dr. Altberg.

A 17 year old male presents to the ED for a seizure. He has never had seizures before. He is currently awake and alert with normal vital signs.

His EKG is below.

1.       What does the EKG demonstrate?

2.       Does this explain the patient’s seizure?

 

ANSWER:

The EKG demonstrates WPW.

WPW can cause arrhythmias which can look like seizures.

 

The EKG demonstrates a sinus rhythm at a rate of approximately 55. The PR interval is approximately 0.10 seconds. There is a delta wave, best visualized in leads V4, V5, V6, II, and aVF. This is consistent with WPW.

WPW is a syndrome of pre-excitation of the ventricles. There is a by-pass tract connecting the atrium and the ventricle which can by-pass the AV node. Normally, when an impulse conducts down the normal conduction system, there is a delay as it passes through the AV node. When an impulse conducts down the by-pass tract, the impulse is not slowed down as it would be if it went through the AV node. So, the amount of time it takes the impulse to get from the atrium to the ventricle is shorter. This is reflected on the EKG by a short PR interval. Once the impulse leaves the bypass tract, it must travel through ventricular myocardium until it reaches normal conduction tissue. So, the impulse travels slower than normal impulses, and is reflected on the EKG by a delta wave and a wide QRS complex.

Patients with WPW are susceptible to tachyarrhythmias. SVT is the most common arrhythmia.

Arrhythmias can cause syncope with some shaking and this may mimic a seizure. So, keep arrhythmia in your differential of patients who present with seizure, especially new onset. As Dr. Reich teaches us, always do an EKG in a patient with new onset seizure.

EKG of the Week 2017 4-30

This EKG comes courtesy of Dr. Hahn.

An 82 year old female presents to the ED complaining of palpitations. She has no chest pain and denies syncope.  Her vital signs are normal.

Her EKG is below.

1.       What is the rhythm?

2.       How would you manage this patient?

 

ANSWER:

The rhythm is sinus with PAC’s. Every third beat is a PAC. This is called atrial trigeminy.

PAC’s usually require no specific management. Patients can be advised to avoid potential triggers such as sympathomimetics, caffeine, Red Bull, etc.

 

The EKG demonstrates an irregular rhythm, but there is a pattern to the irregularity (i.e. it is not irregularly irregular like a-fib). Beat #3 and beat #4 are preceded by P waves and appear to be sinus beats. Beat #5 comes earlier than expected, has a narrow QRS, and probably has a P wave buried in the T wave from beat #4. Thus, it is a PAC. Beats 6 and 7 are sinus, beat 8 is a PAC. Beats 9 and 10 are sinus and beat 11 is a PAC. This pattern continues. When every third beat is a PAC, that is known as atrial trigeminy.  (Every second beat would be bigeminy. Every fourth beat would be quadrigeminy.)

Premature beats can originate from the atria (PAC’s), the junction (i.e. the AV node – called PJC’s) or from the ventricles (PVC’s). PAC’s appear as a P wave which comes earlier than expected followed by a QRS complex that is narrow. Following the PAC, there is a non-compensatory pause. This means that the length from the P wave preceding the PAC to the P wave of the next normal beat is random. It is not related at all to the distance between the normal P waves in the normal beats. This happens because the PAC “re-sets” the SA node. This means, the PAC depolarizes the SA node, so it has to recover before it can generate the next normal beat.

++++PJCs may have a P wave before or after the QRS complex. The P wave will look different than the sinus P waves and it will often be retrograde (i.e. inverted). PJC’s are uncommon in healthy hearts. They occur in CHF, digoxin toxicity, ischemic heart disease, and AMI (especially of the inferior wall).++

PVC’s have no preceding P wave and the QRS complex is wide and bizarre. It looks distinctly different than the other QRS complexes in that lead. Following the PVC, there is a compensatory pause. This means, if you “march out” the P waves, the P waves will continue to arrive at the expected time after the PVC. This occurs because the PVC does NOT reset the SA node. As far as the SA node is concerned, the PVC never happened. So, the SA node continues to fire at its normal pattern.

PAC’s usually require no specific treatment. Patients should be advised to avoid known triggers. These include cocaine, amphetamines, caffeine, Red Bull, pseudoephedrine, etc. Stress is also a common cause of PAC’s.

 

EKG of the Week 2017 4-16

This EKG comes courtesy of Dr. Altberg.

A 19 year old male presents to the ED intoxicated. He also complains of palpitations. His EtOH level is 261. (This is equivalent to a blood alcohol content of 0.26).

His vital signs are: Pulse 140, Respirations 18, BP 120/80.

His EKG is below.

1.       What does the EKG demonstrate?

2.       How would you manage this patient?

ANSWER:

The EKG demonstrates atrial fibrillation. In the setting of acute alcohol intoxication, this is known as Holiday Heart Syndrome.

The heart rate is normal. No specific interventions are necessary. The patient should be observed on telemetry until the a-fib resolves.

 

Patients who “binge drink” are at risk for supraventricular arrhythmias, with atrial fibrillation being the most common. It can also cause atrial flutter, atrial tachycardia, and PVC’s. These patients are typically healthy with no past history of cardiac disease. When they stop drinking, the symptoms go away. This is known as Holiday Heart Syndrome. The arrhythmias can occur at the time of drinking or up to 36 hours later.

Patients with Holiday Heart Syndrome typically present with palpitations. They may also have chest pain and syncope. There are several mechanisms that have been proposed to explain why Holiday Heart occurs.

Initial treatment of patients with Holiday Heart is the same as other patients with atrial fibrillation. If they are tachycardic, their rate should be controlled with AV nodal blockers. However, they are typically at low risk for clots and usually do not require anticoagulation. Rhythm control is usually unnecessary as the arrhythmia usually resolves spontaneously within 24 hours. They should be admitted to a monitored setting.

 

(Tonelo, et al. Holiday Heart Syndrome Revisited after 34 Years. Arq Bras Cardiol. 2013 Aug; 101(2): 183–189.)

(Voskoboinik, Alcohol and Atrial Fibrillation : A Sobering Review. Journal of the American College of Cardiology. Volume 68, Issue 23, 13 December 2016, Pages 2567–2576)

 

Pulmonary Hypertension and Right Ventricular Failure

Mikhail Podlog, DO

Editor: Anna Van Tuyl, MD

 

Introduction/Pathophysiology

The left ventricle (LV) is widely studied and much is known about its normal function, how it performs under stress, and the causes, sequelae, and treatments of LV failure. On the other hand, much less is understood about the right ventricle (RV), including right ventricular failure (1,3). There are many causes of right ventricular failure, the most common being failure of the left ventricle, but one important condition to always consider is pulmonary hypertension (PH), defined as a mean pulmonary artery pressure of 25 mm Hg or higher (1). As pulmonary pressures rise, the increase in afterload on the RV decreases right ventricular stroke volume and output, increasing RV volume.  Since the RV cannot adapt as rapidly as the LV to increases in afterload, this has several detrimental effects on the cardiovascular system.

First, the increased volumes and pressures in the RV causes bulging of the interventricular septum into to LV, decreasing left ventricular preload. This results in a decrease in cardiac output, leading to hypotension and cardiac ischemia (1,3). Second, increased pressures in the RV cause a rise wall tension, decreasing right coronary artery perfusion, which leads to further ischemia. (1,3) Finally, increased pressures in the RV cause tricuspid regurgitation leading to decreased cardiac output (2). All of these processes ultimately cause what is referred to as the right ventricular spiral of death. 

(www.emcrit.org)

(www.emcrit.org)

World Health Organization (WHO) Classifications of Pulmonary Hypertension

Diagnosis

As always, the first step is considering the diagnosis. The most common presenting complaint is exertional dyspnea and pulmonary hypertension should always be thought about if an alternative diagnosis does not explain the patient’s presentation (1). Although a definitive diagnosis of PH requires right heart catheterization, there are several ways ED providers can assess for its presence.

Cardiac Ultrasound
1.    Apical 4 (A4) chamber – RV greater than 2/3rd-1x the size of LV (1,4)
2.    Parasternal short – flattening of interventricular septum, D-shaped LV (1,2)
3.    TAPSE (Tricuspid Annular Plane Systolic Excursion)- M mode through tricuspid annulus in A4 view, >1.6 nml, <1.0 severe dysfunction (7)

CTA Chest  - If RV is greater than 9/10ths of LV, that correlates with increased risk of adverse events and death. (1,4)

Management

Definitive treatment of pulmonary hypertension usually involves treating the underlying causes. This includes diuretics for left heart failure, bronchodilators and steroids for lung diseases, thrombolysis for pulmonary emboli, etc. Appropriate consultations with cardiologists, pulmonologists and other specialists is also emergently indicated for further management. (1,2,3) In the meantime, there are certain things that emergency department providers must do to resuscitate and stabilize the patient in front of them.

Optimize Volume Status

Volume status in these patients is difficult to assess, as the physical exam as well as ultrasound visualization of the IVC is often unreliable. Overloading these patients can lead to further increase in RV volume causing decreased cardiac output and an accelerated path down the spiral of death. Overly diuresing these patients may also lead to a decreased cardiac output if the patient is preload dependent. Here are some tips one can use to assess these patients. (2)

1.     Assume the patient is fluid overloaded and avoid large boluses of fluids -> negative balance is usually key for these patients. (1,2,6)

2.     If there is clear volume loss (diarrhea, blood loss) -> low volume boluses of 250cc of isotonic solution and monitor for effects on blood pressure, heart rate, and urine output.  (1)

a.     If patient is anemic transfuse blood as decreased Hgb and iron has been associated with increased mortality (3,4)

3.     Use passive leg raise maneuver and assess for changes in blood pressure and heart rate (this stimulates giving a bolus and can be rapidly reversed by lowering the legs).

4.     Consider expedited admission to the ICU where a pulmonary artery catheter can be used to obtain accurate central pressures and guide further fluid management, although the efficacy of this is highly debated. (2)

Consider early pressor support

Systemic vasopressors can help prevent the downward spiral of RV failure several ways. Increasing left ventricular afterload can decrease interventricular septum bowing into the LV, increasing cardiac output. Vasopressors also assist in maintaining coronary perfusion to the right ventricle, decreasing effects of ischemia. Although literature is very scant comparing the variety of pressors available, certain pressors have advantages over others in treating pulmonary hypertension.

1.     Norepinephrine – proven benefits in several types of shock; helps maintain coronary perfusion of right ventricle; may increase pulmonary vascular resistance (1,4)

2.     Vasopressin – peripheral vasopressor just like norepinephrine, may actually decrease pulmonary vascular resistance through a NO-induced mechanism (1,2)

3.     Phenylephrine – avoid due to increase in pulmonary vascular resistance when compared to other pressors available (1,5)

4.     Dobutamine – augments myocardial contractility and reduces RV and LV afterload -> increased CO; but disadvantages include decreased SVR and tachycardia so may need to combine with a vasopressor (1,2,3,4)

5.     Milrinone – Unlike dobutamine, PDE3 inhibitors are inotropic and augment cardiac output without chronotropic effects, but disadvantages include decreased SVR as well so may need to combine with a vasopressor; may consider inhaled milrinone if available (2,3,4)

Treat atrial arrhythmias

Patient with pulmonary hypertension are predisposed to atrial tachyarrhythmias. These patients do not tolerate atrial arrhythmias as cardiac output is preload dependent and any minor change can have drastic effects.  Calcium channel blockers and beta blockers should be avoided as they may further impair cardiac function. Cardioversion should always be strongly considered as first line especially for unstable patients (1). Amiodarone can be tried if the patient is stable, and can also be used to pretreat the patient prior to cardioversion. (2,3)

Pulmonary Vasodilations

Pulmonary vasodilators are the only medications that directly reverse the symptom-causing pathology. These are very useful in patients with idiopathic pulmonary hypertension (Category 1) and must be quickly given if a patient is on an IV pump of these medications that has malfunctioned. Inhaled preparations of these medications are also very effective at delivery the medication to highly ventilated portions of the lung, causing local vasodilation and improving V/Q mismatch. Below is a table that lists the categories of pulmonary vasodilators and their potential uses in emergencies.

(1)

(1)

Airway and ventilation management

Maintaining tight control of ventilation and oxygenation is crucial in these patients. Hypoxemia as well as hypercarbic respiratory acidosis can lead to increased pulmonary vasoconstriction, further exacerbating the underlying pathology. Therefore oxygen saturations and carbon dioxide levels in the blood must be maintained in the normal range. (1,4)

If a patient is in respiratory failure, intubation should be avoided at all costs. Intubating these patients can lead to a fatal hemodynamic collapse for two main reasons:

1.     Sedation -> Loss of native catecholamines -> decreased SVR/vasodilation -> decreased venous return -> cardiovascular collapse (1)

2.     Positive pressure ventilation -> increase RV and LV afterload and decreased RV preload -> decreased CO -> cardiovascular collapse (1)

Therefore try to avoid intubating these patients. If respiratory support is needed, first try NIPPV. This avoids the adverse effect of eliminating the patient’s innate catecholamine surge. In addition, the NIPPV can be removed rapidly if the patient begins to deteriorate. (1) If a patient needs to be intubated, following these guidelines can increase your chance of success.

1.     Place an arterial line prior to intubation in order to quickly assess any hemodynamic changes and respond appropriately.

2.     Avoid hypoxia -> preoxygenate the patient and utilize apneic oxygenation during the intubation

3.     Avoid hypercarbia -> induce respiratory alkalosis prior to intubation (4). Hypercarbia worsens pulmonary vasoconstriction.

4.     Consider performing awake intubation.

5.     Medications

a.     Induce with etomidate -> cardiovascular neutral (2)

b.     Paralyze the patient -> increases chances of first pass success

c.     Push dose pressors -> Have ready at the bedside along with your induction/paralytics (1)

d.     Have norepinephrine drip ready -> Have the pump primed and connected; just having the medication in the room is not good enough (1)

6.     Vent settings -> keep intrathoracic pressures low (similar to ARDS protocol) -> low TV, PEEP, low plateau pressures (2,3)

Further management

LVAD, ECMO, atrial septostomy, lung transplant, PH referral center (1,2,3)

References

1.     Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine, Wilcox

2.     Hoeper MM, Granton J. Intensive care unit management of patients with severe pulmonary hypertension and right heart failure. Am J Respir Crit Care Med. 2011;184:1114-1124

3.     Acute Right Ventricular Failure in the Setting of Acute Pulmonary Embolism or Chronic Pulmonary Hypertension: A Detailed Review of the Pathophysiology, Diagnosis, and Management

4.     Lahm T, McCaslin CA, Wozniak TC, et al. Medical and surgical treatment of acute right ventricular failure. J Am Coll Cardiol. 2010;56:1435-1446.

5.     Kwak YL, Lee CS, Park YH, et al. The effect of phenylephrine and norepinephrine in patients with chronic pulmonary hypertension. Anaesthesia. 2002;57:9-14

6.     Ternacle J, Gallet R, Mekontso-Dessap A et al. Diuretics in normotensive patients with acute pulmonary embolism and right ventricular dilatation. Circ J 2013;77:2612–2618.

7.     Schmid E, Hilberath JN, Blumenstock G, Shekar PS, Kling S, Shernan SK, Rosenberge P, Nowak-Machen M. Tricuspid annular plane systolic excursion (TAPSE) predicts poor outcome in patients undergoing acute pulmonary embolectomy. Heart, Lung and Vessels. 2015; 7(2): 151-158

8.     https://emcrit.org/podcasts/pulmonary-hypertension-right-ventricular-failure/

9.     https://www.nhlbi.nih.gov/health/health-topics/topics/pah/types

EKG of the Week 2017 4-2

This EKG comes courtesy of Dr. Adamakos.

An 88 y/o male presented to the ED after syncopal episode. Vital signs: Pulse 40, Respirations 14, BP 130/80. The EKG is below.

1.       What rhythm is demonstrated on this EKG?

2.       How would you manage this patient?

 

ANSWER:

The rhythm is 3rd degree AV block (AKA complete AV block).

The patient is stable. Atropine can be attempted but is unlikely to be successful. Pacing pads should be placed on the chest. A cause of the heart block should be sought.

 

The EKG demonstrates a bradycardic rhythm at a rate of approximately 30. P waves are present but there are dropped P waves. The RR intervals are regular and the PR intervals are irregular. This is consistent with 3rd degree AV block.

Differentiating 2nd degree from 3rd degree AV block can sometimes be difficult. The following algorithm is useful.

If the patient is unstable, they should be treated with a transcutaneous pacer followed by a transvenous pacer. If the patient is stable, reversible causes should be sought. These include hyperkalemia, and toxicity from digoxin, beta blockers or calcium channel blockers. If no reversible cause is identified, the patient will need a permanent pacemaker.