EMS is dispatched to a private residence for 70-year-old female who is believed to be unconscious.

On arrival, the patient is found lying in bed unresponsive to painful stimuli. The patient’s skin is pale and clammy. Her shirt is damp. Snoring respirations are noted and a slow carotid pulse is present.

A medical history is obtained from family members and includes heart failure, stroke, and hypertension.

Vital signs are assessed.

• RR: 8
• HR: Less than 30
• NIBP: 78/41
• SpO2: Not registering
• Temp: 96.1 F / 36.7 C
• BGL: 101 mg/dL

The cardiac monitor is attached.

The adult pads are placed and transcutaneous pacing is initiated.

The patient’s blood pressure improves slightly to 84/47 (confirmed by auscultation). However, paramedics are still concerned about the patient’s hypotension.

Additional treatments

• IO access is obtained in right proximal tibia.
• 0.5 mg of Atropine is administered x 3.
• 9% normal saline is run wide open with an additional IV line established in the left lower extremity.

The patient begins to move and reaches for the pacing pads. However, she is still non-verbal and does not follow commands.

• On arrival at the hospital the patient is transitioned to transvenous pacing.
• She is sent to the cardiac cath lab where a permanent pacemaker is placed.
• In the ICU the patient remains dangerously hypotensive in spite of dobutamine and levophed drips.

The patient eventually expires from multiple-system organ failure.

Discussion

Transcutaneous pacing (TCP) is a difficult skill that is often performed incorrectly. The problem of false capture (also known as echo distortion) is under-recognized and under-reported in the medical literature.

There are many reasons why medical professionals often fail to achieve true electrical and mechanical capture. Consider this excerpt from the Journal of Emergency Medicine where Douglas Ettin, M.D. and Thomas Cook, M.D. describe the difficulty.^[1]

“Shortly after cardiac pacing was initiated, the patient’s systolic blood pressure dropped to 50 mmHg. The EKG monitor continued to demonstrate adequate ventricular capture by the pacer. The patient appeared to have palpable pulses; however, the rhythm contractions of the patient’s body from the pacer shocks made this assessment difficult. With the etiology of the patient’s hypotension unclear, the decision was made to use transthoracic ultrasonography to assess the adequacy of her ventricular contractions.”

“Initially, the ultrasound demonstrated ventricular contractions at a rate of 30-40 beats per minute. These heart contractions did not correspond with the surrounding thoracic muscle contractions generated by the pacer. The current was gradually increased to 110 mA, and the heart began to contract in unison with the pacer shocks. The patient’s blood pressure subsequently increased to 90 mmHg.”

You can see another example where an echo was used to verify capture here.

With false capture, you will generally see a near-vertical upstroke or down-stroke to the “phantom” QRS complex (which is actually electrical artifact created by the current passing between the pacing pads).

You will also note that the underlying rhythm can be seen in the absolute refractory period of one of the (presumed to be) paced QRS complexes (red circle). That is not scientifically possible!

In contrast, true electrical capture will show wide QRS complexes with tall, broad T-waves.

Tips for success

• Perform, but do not rely on a pulse check!
• Use an instrument (SpO2, Doppler, capnography, or echo) to help confirm mechanical capture whenever possible
• Do not be fooled by skeletal muscle contraction!
• Know that the patient may become more alert whether capture is achieved or not
• The most common reasons for “failure to capture” are insufficient milliamperes and poor pad placement!

More examples of transcutaneous pacing (TCP) with capture

Reference

1. Ettin DCook T. Using ultrasound to determine external pacer capture. The Journal of Emergency Medicine. 1999;17(6):1007-1009.

Further reading

Pacing Artifact May Masquerade As Capture

This case was submitted by Roger Hancock with edits by Tom Bouthillet. Some details have been changed to protect patient confidentiality.

A 50-year-old male with a history of hypertension (HTN) and atrial fibrillation (AF) presents to the Emergency Department with complaint of palpitations, which started while mowing the lawn.

He is alert and oriented with a Glasgow Coma Scale (GCS) of 15 and no signs of Hypoperfusion.

• Heart Rate: 165/min, strong and irregular
• Blood Pressure: 140/100 mmHg
• Ventilatory Rate: 22/min
• SpO2: 98% on room air

The patient is compliant with his medications and denies any allergies.

A 12 Lead ECG is recorded.

The patient was treated with 20 mg of diltiazem (Cardizem) over 2 min, followed by 10 mg over 1 hr, and 0.25 mg digoxin (Lanoxin).

A rhythm change was noted on the monitor and another 12-lead ECG was recorded.

The patient was now asymptomatic and admitted for observation without further incident.

Understanding Diltiazem (Cardizem)

Diltiazem (Cardizem) is a Class IV antiarrhythmic and one of the most common pharmacological agents used for treatment of AF with RVR.

Class IV antiarrhythmics are Calcium Channel Blockers (CCBs), which inhibit intracellular calcium influx via calcium channel antagonism. These particular pharmacological agents can be further divided into subdivisions based on their molecular composition:

Dihydropyridines (DHPs)

• These CCBs can be easily identified by the last four letters of the generic name ending with “pine”.

• DHP CCBs are more selective to peripheral vasculature than cardiac cells, leading to arterial smooth muscle relaxation and decreased Systemic Vascular Resistance (SVR), thus, decreasing afterload and Myocardial Oxygen Demand (MVO2).

• Because of this peripheral calcium channel selectivity, they are commonly used for treatment of Hypertension and angina.

• Their hemodynamic effects can be associated with adverse effects such as hypotension and reflex tachycardia secondary to sympathetic stimulation as a compensatory mechanism for the decreased cardiac output.

Examples include:

• Amlodipine (Norvasc)
• Nicardipine (Cardene)
• Nifedipine (Procardia)

Non-dihydropyridines (NDHPs)

• These CCBs are those which generic name does not end with “pine”.

• Can be further divided into benzothiazepines (not to be confused with benzodiazepines) and phenylalkylamines.

• Non-dihydropyridine CCBs are more selective to L-Type Calcium Channels in cardiac cells, such as the Sino Atrial Node (SAN) and Atrio Ventricular Node (AVN), although all CCBs cause peripheral vasodilation.

• This Calcium Channel antagonism leads to decreased SAN chronotropic effect and decreased AVN conduction, making it useful for treatment of atrial arrhythmias such as AF, Atrial Flutter and Supra-ventricular Tachycardias (SVTs).

Examples include:

• Benzothiazepines: Diltiazem
• Phenylalkylamines: Verapamil

Vaughan-Williams Anti-arrhythmic Classification

There are four specific classes of antiarrhythmics with specific physiological functions divided into classes based on their mechanism of action. The rest of the pharmacological agents used as antiarrhythmics fall under the fifth class with different mechanisms of action from the previous classes.

One important aspect to understand is that although they are all antiarrhythmics, each class works under different mechanisms and therefore may have different effects on cardiac cells. Some target atrial, AV nodal or ventricular cells, while some have the capacity to address both atrial and ventricular arrhythmias.

Pharmacological Use

Diltiazem has a COR I, LOE-b classification, used for rate control of atrial arrhythmias, predominantly Atrial Fibrillation, and COR IIa, LOE-b for treatment of SVT with a reentry pathway mechanism.

Mechanism Of Action

• Negative Chronotropic, Inotropic and Dromotropic effect by blocking L-Type Calcium Channels in cardiac tissue

• Decreased Calcium influx affects Phase 2 of cardiac depolarization, delaying atrial and AVN conduction

• This ultimately leads to decreased ventricular rate, with or without conversion to sinus rhythm

Caution

• Diltiazem should be avoided in the presence of pre-excited AF with RVR, that is, AF in the presence of accessory pathway, i.e. Wolff Parkinson White (WPW) syndrome, as AVN blockage can lead to increased conduction through the accessory pathway, leading to life-threatening rapid ventricular rates.

• Procainamide and Ibutilide are the preferred treatment of pre-excited AF with RVR and hemodynamically stable patients.

• Diltiazem can be used in patients with AF and Heart Failure (HF) but with caution in reduced Left Ventricular Ejection Fraction and hypotension.

Dose and Administration

Although dosages may vary based on physician orders, protocols and age, a standard initial dose is 0.25 mg/kg, ranging between 10-20 mg over 2 minutes, with a second dose of 0.35 mg/kg, ranging between 20-25 mg over 2 minutes, often followed by a 5-10 mg/hr infusion.

Treatment of hemodynamically unstable patients in narrow QRS complex AF with RVR requires synchronized cardioversion at 120-200 J initially, and should not be delayed for administration of an anti-arrhythmic agent.

Conclusion

• Diltiazem is a Class IV, non-dihydropyridine CCB anti-arrhythmic, serving as the most common pharmacological agent used for the treatment of AF and SVTs, for patients that are hemodynamically stable.

• Caution should be used with CCBs and HF with decreased EF and hypotension.

• Electrical Cardioversion should not be delayed for treatment with an anti-arrhythmic agent in the presence of Hypoperfusion and hemodynamically unstable patients.

Bag mask ventilation is the cornerstone of airway management.

It’s often considered a basic procedure, but there is nothing “basic” about BVM ventilation. Skill acquisition requires extensive training and experience. It’s not pretty, sexy, or glamorous. Most people perform it poorly even though it’s an essential part of good airway management.

We often relegate the skill to a new or junior provider, and when the saturation drops we attribute it to the patients’ acuity and not to failure to provide adequate oxygenation and ventilation.

The AHA recognizes that bag mask ventilation “is a challenging skill that requires considerable practice for competency.”

When performed in an emergency, respiratory failure or arrest is often imminent. Because it is a BLS skill we toss a BVM to our partner while we prepare our intubation equipment. The mask is placed on the patient’s face and ventilations are administered too aggressively or ineffectively.

When this is not recognized the airway may become flooded with gastric contents during the intubation attempt making more difficult if not impossible. Aspiration occurs, hypoxia worsens, and the patient is at higher risk of experiencing cardiac arrest.

It is not widely appreciated that BVM ventilation is often ineffective. One assumes that it works better than it actually does without appreciate education and training, which is often lacking.

Early in my career I would place the mask on the patient’s face and apply the CE technique without any objective measurement of how well it was working.

How do you Know When Ventilations are Effective?

Clinical detection of adequate ventilation is notoriously difficult. So what is the litmus test for gas exchange at the alveolar level? ETCO2 of course!

In Emergency Medicine we want the technique that is most likely to be successful the first time. The traditional CE method is not always the best technique. Some will be quick to contest that assertion, and a few years ago I would have agreed with you.

Then I watched a video on EmCrit made by Reuben Strayer.

There are three main factors that contribute to poor BVM ventilation.

• Poor mask seal
• Improper positioning
• Excessive rate and volume

Poor Mask Seal

When using the traditional CE technique, pressure is not distributed equally across the mask. This means that when using your left hand, there is a tendency for air to leak between the mask and the right side of the patient’s mouth, which often goes unrecognized.

Improper Positioning

Because of the inherit difficulty maintaining a quality seal, and because maintaining a seal is fatiguing, the tendency is to push the mask onto the face. The mouth is then closed shut, leaving the nares as the only route of ventilation. Obstructive soft tissues of the pharynx collapse, blocking the glottic opening.

A superior technique was introduced 11 years ago in the 2005 AHA Guidelines.

“Bag-mask ventilation is most effective when provided by 2 trained and experienced rescuers. One rescuer opens the airway and seals the mask to the face while the other squeezes the bag. Both rescuers watch for visible chest rise.”

The two handed technique is sometimes referred to as the thenar eminence (TE), or “two thumbs down” technique.

Gerstein (2013) compared the effectiveness of the CE and TE technique when performed by novice clinicians and found:

“The TE facemask ventilation grip results in improved ventilation over the EC grip in the hands of novice providers.”

A few weeks ago I attended a cadaver lab in Baltimore. The first skill we practiced was BVM ventilation. Our group leader has us try the CE technique first, then TE. The chest was open and lungs exposed so we could see the effectiveness of our ventilations.

Six people were in my group, and no one was able to inflate the lungs using the CE technique despite multiple attempts. However, the lungs were inflated every time, every attempt, for every person when using the TE technique!

Excessive Rate and Tidal Volume (Hyperventilation)

Even when trying to be cognizant of rate and tidal volume, there can be a huge difference in what you think you’re doing, and what you’re actually doing.

This was proven in the Milwaukee study, in which Paramedics were taught to ventilate at the appropriate rate during cardiac arrest. They retrospectively looked at the ventilation rates objectively and found the average rate was 30 breaths/min!

An excessive rate and tidal volume isn’t only deleterious for patients in cardiac arrest, but increases the likelihood of exceeding the pressure of the lower esophageal sphincter, delivering large tidal volumes of air to the stomach.

This also was mentioned back in the 2005 AHA Guidelines:

“Gastric inflation often develops when ventilation is provided without an advanced airway. It can cause regurgitation and aspiration, and by elevating the diaphragm, it can restrict lung movement and decrease respiratory compliance. Air delivered with each rescue breath can enter the stomach when pressure in the esophagus exceeds the lower esophageal sphincter opening pressure. Risk of gastric inflation is increased by high proximal airway pressure and the reduced opening pressure of the lower esophageal sphincter. High pressure can be created by a short inspiratory time, large tidal volume, high peak inspiratory pressure, incomplete airway opening, and decreased lung compliance.”

To prevent gastric inflation the airway must be kept open, and breaths delivered slowly…very slowly. Based on my observations no one delivers breaths slow enough. When your own heart rate is going 150 beats per minute, waiting 6 seconds to deliver a breath feels like forever! I often tell someone who is bagging to fast to deliver a breath every 10 seconds and even then they often ventilate too fast.

How do we slow down? Well, if the patient is intubated they could be placed on the ventilator. But since we’re talking about facemask ventilation, consider purchasing a timing light that goes on the end of the BVM, or use a metronome. You could also try counting, “one, one thousand…two, one thousand…three, one thousand…” and so on.

In addition to delivering breaths too fast, we deliver too much. The average volume of an adult BVM is 1600 milliliters! Squeezing the bag until opposite sides of the BVM touch isn’t necessary! It’s recommended that only 1/3 of the bag be compressed to give a large enough tidal volume. Any more and the pressure is too much for the rigid trachea to accommodate, and the esophagus is more than happy to accept the rest!

BVM Ventilation during Cardiac Arrest

If you’re doing 30:2 during BLS CPR you don’t have the luxury of providing breaths slowly. The goal should be to have compressions resumed within 3 seconds, and to do that the breaths can’t be given quickly or it will take 5 or 6 seconds!

The goal should be “little bag squeeze, little bag squeeze” with full release between squeezes. Intrathoracic pressure stays elevated without a full release, and we know that increased intrathoracic pressure impedes venous return.

Conclusion

• BVM ventilation is a difficult skill for providers at all levels and specialties.
• The traditional CE method is not very effective, and sometimes totally ineffective.
• Use ETCO2 as an objective measurement.
• Adopt the “two thumbs down” technique
• Deliver breaths slowly
• Only compress 1/3 of the bag
• Give breaths quickly during cardiac arrest, but allow full release of BVM

References
“Beginner Facemask Ventilation Techniques | Emsworld.Com”. EMSWorld.com. N.p., 2016. Web. 17 Mar. 2016.
Gerstein NS, et al. “Efficacy Of Facemask Ventilation Techniques In Novice Providers. – Pubmed – NCBI”. Ncbi.nlm.nih.gov. N.p., 2016. Web. 17 Mar. 2016.
“Part 4: Adult Basic Life Support”. Circulation 112.24_suppl (2005): IV-19-IV-34. Web. 17 Mar. 2016

EMS is called to the home of a 62-year-old female who complains of shortness of breath and epigastric discomfort.

On their arrival, they find the patient sitting on a chair in her living room, holding her hand to her chest while she talks with first responders. She is not pale, but appears diaphoretic, anxious, and has mildly laboured respirations.

A brief medical history is obtained while gathering a set of vitals and applying the ECG electrodes.

Onset:              “It woke me up from my sleep”
Provocation:   “Nothing makes it better or worse”
Quality:            “Like heartburn, but worse”
Radiation:        None
Severity:           Rated 8 out of 10
Time:                “About ninety minutes ago”

Pulse:              74/min, strong and regular at the wrist
RR:                  20/min, clear air entry on auscultation
NIBP:              152/88
SpO2:              92% on room air
BGL:                7.4mmol/L (133 mg/dl)
Temp:             36.2C (97.2F)
PMHx :           Hypertension, asthma, dyslipidemia

A 12-lead ECG is acquired.

At this point, the attending paramedic was highly suspicious that an acute coronary event was taking place, and proceeded to treat with Aspirin, SL Nitroglycerin, and serial 12-leads while initiating transport.

The following ECG was acquired with V4 moved to the position of V4R, and V5 & V6 moved to the position of V8 & V9, respectively.

The transporting paramedic recognized the posterior STEMI and transmitted the ECG to a consulting physician. Based on these findings, and considering the significant distance to a PCI-capable facility, the decision was made to administer Plavix and IV thrombolytics (TNK).

About 20 minutes post-TNK, it was noted that the patient’s heart rate had decreased to the low 40’s, while her chest discomfort simultaneously improved.

The following 12-lead was acquired.

Despite the precipitous drop in blood pressure and heart rate, the patient appeared healthier now than she had at any point previously during the encounter.

Does this ECG represent improvement, or a decline in clinical condition?

Posterior STEMI

The diagnosis of a truly isolated posterior STEMI appears to be a relatively uncommon occurrence, presenting in about 3% of myocardial infarctions ¹, however it’s highly likely that underdiagnosis has played a role in these underwhelming stats. This may be due to a misconception by many practitioners that ST Depression (STD) in leads V1-V3 represents anterior ischemia, despite the fact that myocardial ischemia does not localize on the 12-lead ECG.

This misinterpretation, combined with arbitrary millimeter criteria, often result in delayed cath lab activation, or a diagnosis of UA/NSTEMI in patients who are in fact suffering acute posterior STEMI.

There are several key criteria on the 12-lead ECG that, when observed in a patient suffering from a suspected acute coronary syndrome, should lead you to make the diagnosis of posterior STEMI. They include:

• Horizontal ST depression in V1-V3 with upright T-waves
• Early R-wave progression in the precordial leads
• ≥ 0.5mm ST Elevation (STE) in one or more posterior leads (V7-V9)*

* Due to the anatomical structures located between the posterior leads and the heart, there’s an increased amount of electrical impedance, which results in the appearance of much smaller QRS complexes in the posterior leads. This is why half of a millimeter of STE is significant in these leads!

However, these low-voltage leads can make ST-segment elevation difficult to appreciate, which has the potential to confuse the diagnosis. As a result, some experts suggest that the diagnosis of posterior STEMI can and should be made using the other two criteria alone.

Prehospital Thrombolytics

Over the last ten years, the use of thrombolytics in the prehospital arena has increased significantly around the world, especially in rural and remote communities.

While primary-PCI within 120 minutes of first-medical contact (FMC) remains the ideal pathway for patients with acute STEMI, a combined pharmaco-invasive approach has been suggested to be comparably effective in reducing morbidity/mortality in patients presenting with acute STEMI in regions that cannot provide primary-PCI.

In these cases, patients are treated with intravenous fibrinolytics, usually following ECG transmission, expert consultation, and careful screening processes. Following this, the patient is promptly arranged transport to a PCI center where rescue catheterization or follow-up angiogram can be completed.²

With the goal being to minimize infarction size and myocardial necrosis, many services have implemented protocols that allow for EMS administration of fibrinolytics. This has been shown to significantly reduce the time-to-treatment when compared to services which transport to the closest facility prior to the administration of fibrinolytics.³

When paramedics are given the appropriate level of training and equipment, prehospital fibrinolysis can be an effective and efficient means of reducing total ischemic time, and efforts should be made to lobby for this intervention in regions which cannot meet the 2-hour PCI window.

Reperfusion Arrhythmias

Between 80-90% of STEMI patients who receive either PCI or thrombolytics will experience some form of reperfusion-related arrhythmias within the first 48 hours of treatment.

With the expanding utilization of thrombolytics for acute STEMI, the occurrence of these “reperfusion rhythms” has become increasingly common in prehospital and ED settings alike. These rhythms most commonly occur when oxygenated blood begins flowing through previously occluded coronary arteries, and while it’s uncertain what degree of coronary artery patency they represent, it’s generally accepted that these arrhythmias represent some degree of myocardial reperfusion.⁴

Slower reperfusion arrhythmias such as sinus bradycardia and ventricular escape rhythms are thought to be resultant of increased vagal tone in the recently ischemic myocardial tissue; a phenomenon known as the Bezold-Jarisch Reflex, which is most commonly seen in inferior or posterior MI’s.⁵

These slow rhythms often occur alongside periods of frank hypotension, however these incidents are most often self-limiting and well tolerated, and may in fact occur at a time when the patient reports finally feeling better! Consequently, aggressive interventions to increase the heart rate are rarely required, and can usually be limited to postural changes or the administration of atropine, or very rarely transcutaneous pacing. ⁷

Faster reperfusion arrhythmias may include frequent premature ventricular complexes, accelerated idioventricular rhythm, or nonsustained runs of ventricular tachycardia. These “irritable” rhythms  are thought to originate from the zone of ischemia, which surrounds the zone of infarction, where “overactive” calcium channels are believed to play a significant role. The arrhythmia may be occurring as a result of an ectopic foci, or serving as an escape rhythm when the sinus node is depressed (perhaps due to the vagal response mentioned above).

Recent research suggests that the presence of these arrhythmias may predict a larger area of infarction, or possibly incomplete or poor reperfusion (TIMI flow grade <3). Management of these patients should be aimed primarily at continuous cardiac monitoring and hemodynamic support to maximize myocardial perfusion, with use of antiarrhythmic drugs to be considered further down the treatment algorithm.

References

1. Oraii S, Maleki M, Abbas Tavakolian A, et al. “Prevalence and outcome of ST-segment elevation in posterior electrocardiographic leads during acute myocardial infarction.” J Electrocardiol 1999;32: 275-8 http://www.ncbi.nlm.nih.gov/pubmed/10465571
2. Danchin N, Durand E, Blanchard D, “Pre-hospital thrombolysis in perspective.” European Heart Journal. DOI: http://dx.doi.org/10.1093/eurheartj/ehn462 2835-2842 First published online: 23 October 2008
3. McCaul M, Lourens A, Kredo. “Pre-hospital versus in-hospital thrombolysis for ST-elevation myocardial infarction.” Cochrane Database Syst Rev. 2014 Sep 10;9:CD010191. doi: 10.1002/14651858.CD010191.pub2 http://www.ncbi.nlm.nih.gov/pubmed/25208209
4. Ersan Tatli, Güray Alicik, Ali Buturak, Mustafa Yilmaztepe, and Meryem Aktoz, “Arrhythmias following Revascularization Procedures in the Course of Acute Myocardial Infarction: Are They Indicators of Reperfusion or Ongoing Ischemia?,” The Scientific World Journal, vol. 2013, Article ID 160380, 7 pages, 2013. doi:10.1155/2013/160380 http://www.hindawi.com/journals/tswj/2013/160380/cta/
5. Koren G, Weiss AT, Ben-David Y, Hasin Y, Luria MH, Gotsman MS. “Bradycardia and hypotension following reperfusion with streptokinase (Bezold-Jarisch reflex): a sign of coronary thrombolysis and myocardial salvage.” http://www.hindawi.com/journals/tswj/2013/160380/cta/
6. Gulumser Heper, Mehmet Emin Korkmaz, Ayhan Kilic, “Reperfusion Arrhythmias: Are They Only a Marker of Epicardial Reperfusion or Continuing Myocardial Ischemia After Acute Myocardial Infarction?” ANGIOLOGY 2008 vol. 58 no. 6 663-670  doi: 10.1177/0003319707308891  http://ang.sagepub.com/content/58/6/663
7. Esente P, Giambartolomei A, Gensini GG, Dator C. “Coronary reperfusion and Bezold-Jarisch reflex (bradycardia and hypotension)”, Am J Cardiol. 1983 Aug;52(3):221-4. http://www.ncbi.nlm.nih.gov/pubmed/6869265

Unfortunately not every patient that suffers a STEMI makes a complete recovery, even if treated with primary PCI. Patients that present late into their infarct have a higher risk of developing a complication.

Here are two cases that illustrate the spectrum of mechanical complications that can occur in the aftermath of an infarct.

Case 1

A 53 year old lady with hypertension and hypercholesterolaemia called an ambulance about 8 hours after the onset of her chest pain.

Vital signs are assessed.

BP: 100/60
HR: 96bpm

The pre-hospital ECG traces obtained by the paramedics are shown:

Both ECGs show clear inferior ST elevation with prominent Q waves. There is reciprocal change anterolaterally but importantly for an inferior MI, heart rate is normal. The ECGs are 50 minutes apart and the changes appear to be slightly worse on her second ECG, but not drastically.

She was still in pain on arrival at the interventional centre and transferred immediately to the cath lab. Her left system showed moderate disease in the circumflex artery. However, as expected, the acute problem was her right coronary artery, which was occluded.

Below you can see the guide catheter engaged with the blocked right coronary artery and no flow is getting past the clot.

A thin angioplasty wire is passed through the thrombus and to the distal vessel. The thrombus was more resistant (i.e. mature) than most acute infarcts, which fit with the 8 hour history of pain.

You can see even passing a 0.014” diameter wire restores some flow. The wire tip is in the posterior descending artery. Reperfusion is often when patients destabilise and indeed the patient’s heart rate dropped to 20bpm and blood pressure to 60mmHg but she responded quickly to atropine and fluid. In the proximal vessel, a filling defect can be seen which is a sizeable thrombus.

A 3.5mm wide and 38mm long drug-eluting stent was placed without complication in her RCA, producing a nice angiographic result. However, the long period of coronary occlusion may well have caused significant myocardial injury. She was kept under close observation.

A satisfying sight for any healthcare professional is seeing a patient’s ST elevation resolve after opening their artery. However, her post procedure ECGs revealed persistent ST elevation.

You can see the evolution of her infarct as the deeply inverted inferolateral T waves revert but her STs remain elevated and develop a more mature ‘rounded’ appearance.

She returned to the ward but deteriorated. Inferior STEMIs carry a more favourable prognosis than anterior (as LV function is normally not as dramatically affected), so clinical instability post procedure should be a concern. On examination she was pain-free but breathless:

RR 24
SO2 92% 2L O2
HR: 80bpm
Chest auscultation: crackles bibasally
Heart sounds: loud pansystolic murmur

A bedside echocardiogram was performed.

A parasternal long axis view reveals the posterior mitral valve leaflet is tethered. The basal posterolateral wall is hypokinetic.

A close up of the valve with colour Doppler demonstrates mitral regurgitation.

An apical 4-chamber (zoomed in) shows the mitral regurgitation is significant.

This parasternal short axis view gives the clearest demonstration of the problem. A regional wall motion abnormality is clearly seen affected the infero-septum and inferior wall. The rest of the left ventricle is contracting well.

Her chest radiograph confirmed the clinical suspicion of pulmonary oedema and she was treated with diuresis. She responded well.

Why did the patient develop pulmonary oedema?

The papillary muscles are very strong muscles connected to the mitral valve to prevent it inverting during ventricular systole. There are two papillary muscles in the left ventricle, each connected to a mitral valve leaflet.

The anterolateral papillary muscle is connected to the anterior mitral valve leaflet and receives a blood supply from both the left anterior descending artery (via a diagonal) and the circumflex artery (via an obtuse marginal). However the posteromedial papillary muscle only has one blood supply, which is the posterior descending artery, a branch of the right coronary artery in 90% of people.

Therefore one can appreciate why mitral valve problems are more common following an inferior STEMI. In this case an almost akinetic segment, which included the posteromedial papillary muscle, caused the posterior mitral valve leaflet to become fixed, causing mitral regurgitation. Even though overall left ventricular function was only mildly impaired on the echocardiogram, the regurgitant pressure into the lungs can precipitate pulmonary oedema.

In more severe cases, the papillary muscle may rupture completely causing a ‘flail leaflet’ and catastrophic mitral regurgitation. It is often fatal. This complication typically occurs 2-7 days following a myocardial infarction, so if a patient suddenly deteriorates in the days after an MI, check for a murmur and organise an urgent echocardiogram. They can develop cardiogenic shock within minutes.

Case 2

An 80 year old man suffered a severe episode of chest pain but did not seek medical attention until about 2 weeks later, by which time he’d become progressively more breathless. His primary care doctor heard a loud, previously undocumented murmur and referred him into hospital.

On examination, in addition to the murmur, he had signs of right sided heart failure with an elevated JVP and peripheral oedema. His ECG revealed inferior Q waves.

Parasternal long axis view: The septum is moving in an unusual jerky fashion and something can be seen in the RV. Despite left ventricular function appearing reasonable, the aortic valve is not opening much suggesting cardiac output is low.

Parasternal short axis: There is a large ventriculo-septal defect in the infero-septal LV. The right ventricle is severely impaired.

Apical 4 chamber:

The LV function is hyperdynamic. The infero-basal septum is tethered near the mitral and tricuspid valves but highly mobile, creating a large VSD. The right ventricular free wall appears to bulge out and the RV is almost akinetic.

Apical 4 chamber colour Doppler:

There is free flow between LV and RV.

Apical 2 chamber. This view demonstrates the bulging from the RV also appears to involve the LV. This is a sealed perforation with aneurysm formation.

In this remarkable loop, the echo probe moves and one can clearly appreciate the defect in the septum, along with the thin membranes sealing the perforation.

What happened?

In addition to problems with the mitral valve, ventricular perforation and ventriculoseptal defects (VSDs) are the two other catastrophic mechanical complications of an MI. LV wall rupture typically occurs in the first 5 days, but some can be as late as a fortnight later. In this case, it is unclear when the complication occurred.

Complete free wall rupture rapidly leads to tamponade and death, but a sub-acute perforation refers to one that has been sealed with thrombus or the pericardium. This remains very high risk for subsequent complete rupture. Somewhat paradoxically the risk of developing any mechanical complication is not proportional to the size of the infarct and small infarcts can pose a large risk.

This patient suffered both a large VSD and a sealed perforation of the inferobasal free wall.

Management

These patients may present in cardiogenic shock and should be managed accordingly. Treatment might include diuresis, vasopressors, inotropes, intra-aortic balloon pump or mechanical cardiac support. The only definitive treatment is invasive, but these patients are exceedingly high risk and optimal timing can be very hard to judge. Most patients will be considered for early surgery but percutaneous closure of VSDs is increasing, to avoid the risk of a general anaesthetic.

Summary

• There are three mechanical complications of acute myocardial infarction: acute mitral regurgitation, VSD and LV rupture
• They typically occur 2-7 days following an MI
• Have a high index of suspicion if a patient presents following an MI with a sudden deterioration
• Symptoms and signs include breathlessness, right-sided heart failure and a new harsh pansystolic murmur
• Urgent echocardiography is indicated and diagnostic in most cases
• Treatment is supportive and surgical

References:
Mechanical complications of acute myocardial infarction, accessed 26^th February 2016. Available at: http://www.uptodate.com/contents/mechanical-complications-of-acute-myocardial-infarction