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Spontaneous Circulation
Spontaneous Circulation focuses on advanced ECG interpretation, cardiac pharmacology, hemodynamic assessment and resuscitation, and managing acute coronary syndrome. It is devoted to translating the best evidence-based treatments from critical care, resuscitation, and trauma for bedside use in the emergency department.
Monday, February 02, 2015

We physicians are obsessed with classifying, sorting, and differentiating in a quest for never-ending precision. We gather all manner of “facts” from our patients. Sights, smells, reactions to pushing or pulling. We divine sounds with antiquated stethoscopes or peer underneath the skin with ultrasound. We subject them to tests of blood, urine, and fluids from any place our needles can reach.



All of this is to arrive at an exact diagnosis that is often frustrated by the secondary nature of the data. Our disappointment has driven us mad, but the promise of exactness from biomarkers leaves us giddy. We have convinced ourselves that these laboratory tests will provide us the dichotomous yes/no answers we tell ourselves that our patients demand, but is really more for us. Answers without all of the messiness.


Does the patient have pneumonia? Check procalcitonin. Want to know if he has a pulmonary embolism? How high is the D-dimer? Why is the patient short of breath? Better get a BNP level. Chest pain? Run a troponin level (three times every four hours).


Troponins have turned on us, however, and emergency physicians and cardiologists are quickly learning to hate their old friend. Troponin levels were such a good biomarker. Positive levels were a clear marker of acute myocardial infarction; negative values ruled out the diagnosis. Exactly what we wanted from a biomarker. As the clinical chemists devised ways to measure troponins at lower and lower levels, however, we started to find patients with positive troponin levels who were not having acute coronary syndrome (ACS). Deciphering the meaning of a positive troponin is becoming less clear, making our lives messy again.


Troponin is found as a complex (troponin I, troponin C, troponin T) in myocardial cells that displaces tropomyosin when activated by entering calcium, exposing binding sites on actin for myosin. In short, troponin forms the trigger mechanism that starts heart cells contracting, two fortunate facts that make it useful as a marker. First, there is a version of troponin I and T that are only present in myocytes. Second is that the cardiac form of troponin is about 50 percent different from the skeletal muscle version. These two facts together mean that we can specifically measure the cardiac version, and that any way we measure we know is coming from the heart, not skeletal muscle.


Intracellular troponin is mostly bound as a complex (94%) attached to tropomyosin with only 6% free in the cytosol. It must be released from the cell for us to measure troponin levels in the blood. This has traditionally been assumed only to occur when cells die and leak their contents, but several alternative mechanisms are likely. First, there is natural turnover of myocardial cells. About 40 percent of all myocytes will turn over (programmed cell death can occur as apoptosis or autophagy) during a person’s life. The troponin proteins wear out, and are degraded by proteasomes within the cell cytoplasm into fragments. These can be released and measured by the assays. Lastly, oxidative stress can increase cell wall permeability or cause formation of cellular blebs, allowing for the release of fragments and free cytosolic troponin. These mechanisms mean that even normal individuals have measurably low troponin levels, which we can now detect as our assays have become more sensitive.


Once troponin is released from the cell, its half-life (t½) is approximately 120 minutes before it is cleared renally. Troponin can continue to be measured for longer periods after an insult because there is continued released from the myofibrillar pool as myocytes continue to undergo degradation during necrosis.


The original troponin assay was developed in 1987. Unlike measurement of CK-MB, an enzymatic assay, troponin is a protein, and assays use a sandwich ELISA method. The capture antibody has binding sites directed at cardiac-specific epitopes on the troponin molecule. The detection antibody binds different epitopes to increase specificity. Determining which epitopes to target is dependent on the manufacturer, but no two antibody pairs can have 100% sensitivity because of their existing troponin fragments, post-translational modifications, oxidation, phosphorylation, and complexes.


So what defines a high-sensitivity test? The important point to remember is that we are talking about analytical sensitivity, not clinical sensitivity. The sensitivity of detecting troponin, not how useful that measurement is, answers our clinical questions, such as whether the patient is having a myocardial infarction. Two criteria have been established for assays to be labelled high-sensitivity. The first is that it must be able to measure a detectable value for 50% of healthy individuals. This is called the limit of detection. The second criterion is coefficient of variation (CV). This is the analytical impression at the 99% percentile. Most contemporary tests are about 20%, and high-sensitives are generally much better. The lower sensitivity is important, but the more precise CV may actually be more clinically useful because it makes troponin measurements easier to repeat, especially at the lower values. Table 1 lists generations of troponin assays, and Figure 1 provides a visualization of the assay criteria.



Manufacturers reengineered the detection antibody to meet the criteria of high-sensitivity assay. They also increase the sample volume, raise the ruthenium concentration, and optimize the buffer to reduce background noise.


A challenge that manufacturers face is defining what constitutes a healthy population and establishing the 99th percentile upper limit normal (ULN). The normal has age and sex variations. Some manufacturers obtain only a health questionnaire (ranging from simple to extensive), while others perform a physical exam, ECG, and echocardiogram. How the healthy population is defined can have significant effects on the normal limits established. There are no guidelines, but current recommendations suggest establishing one cohort of patients under age 30 and another over age 30 with a median age of 60-65. A detailed history should be taken, the blood should be measured, and BNP should be obtained to screen for cardiomyopathy. Of course, patients included should have an equal sex and racial mix. At least 400-500 individuals are needed to obtain a statistically valid sample.


Using the high-sensitivity assays in healthy populations, we have started to notice significant biologic variability. That is variation of troponin levels over a day and other cycles, which may become important when assessing serial measurements as part of evaluations.


After all of this work developing a more advanced troponin assay, we are at least left with something very useful. Well, maybe. Before we can answer the clinical usefulness of high-sensitivity troponins (PPV of hs-cTn measurements), we need to understand the definitions and mechanisms of myocardial injury and infarction. Myocardial injury involves cell death, and is indicated by positive troponins. Many mechanisms can cause cell death, however. The myocardial cells become ischemic if they are deprived of adequate oxygen supply, and an infarction can develop if that persists long enough.




But as we know, the clinical presentation of myocardial infarction can vary tremendously, and arriving at a diagnosis can be challenging. A consensus conference has determined diagnostic criteria for myocardial infarction. In the most recent version from 2007, there must be evidence of positive troponins that have a rise/fall pattern indicating acute process with at least one value above the 99th percentile ULN. This must be supported by the appropriate clinical context and either ECG, imaging, or angiography evidence.





Myocardial infarction can be subdivided into subtypes. Type 1 is what we typically think of with the term myocardial infarction — plaque rupture and formation of an intracoronary thrombus. This is an acute coronary syndrome. Type 2 myocardial infarction occurs when there is a temporary imbalance between the perfusion and cardiac oxygen demand. This leads to ischemia and can cause an infarction and necrosis without a plaque rupture or thrombus formation. By definition, this is not an acute coronary syndrome despite the presence of elevated troponins, so it is important to note that myocardial infarction is not synonymous with ACS. Types 3, 4, and 5 are less useful for emergency physicians.



Elevated troponins can also occur because of nonischemic mechanisms that cause direct myocardial damage. The troponins indicate cell death with necrosis, but ischemia was not the mechanism. Examples include cardiac contusion, myocarditis, malignancy, and sepsis.




Unfortunately, distinguishing between type 1 MI, type 2 MI, and nonischemic myocardial injury can be challenging, especially in coronary artery disease. Troponins were found to be more sensitive than CK-MB in those found to have myocardial necrosis, and there is a level-dependent increasing risk for adverse outcomes. The elevation itself, however, does not provide any information about etiology. It does indicate myocardial injury, but it fails as an absolute biomarker for acute myocardial infarction. Clinical context is very important, and the entirety of the clinical presentation (history, physical exam, ECG, imaging, and angiography) matters in determining the diagnosis. The dynamic rise and fall of troponins on serial measurement can help establish that there has been an acute myocardial injury, rather than a baseline troponin elevation as may be seen in renal failure. A diagnosis of type 2 MI should be considered only when there is clinical evidence of an acute imbalance. Nonischemic mechanisms should be evident from the history. Ultimately in cases where the diagnosis remains uncertain, advanced imaging such as cardiac MRI may be useful.


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Tuesday, December 09, 2014

Nursing home staff became concerned about a patient because he was “floppy.” He was a 59-year-old man with stage 3 chronic kidney disease, right ventricular heart failure, hypertension, cirrhosis, and insulin-dependent type 2 diabetes mellitus. He had been sleeping all day, according to his nurse, but he was not responding when she checked on him in the evening, and she could “drop his arm and it would just hit his face.”


He was hypotensive (90/50 mm Hg) and bradycardic (about 30 beats/min) in the ED. Respirations were slow and shallow. He was protecting his airway, but was hypoxic (SpO2 82%). IV access was established, and initial laboratory tests were sent. He was orotracheally intubated without difficulty and easily ventilated. Atropine was given, but did not increase his heart rate. The symptomatic bradycardia meant starting transcutaneous pacing. Fingerstick glucose was 174 mg/dL. Given his history of kidney disease and diabetes mellitus, there was a high suspicion for hyperkalemia so he was empirically treated with calcium gluconate and shifted with insulin/glucose. It was difficult to get good electrical capture with the transcutaneous pacing. Multiple different pad locations were attempted, and eventually we were able to achieve intermittent capture using pads in the right-parasternal and apex position.


A 12-lead ECG was obtained that demonstrated sinus bradycardia with a narrow QRS complex and no T-wave abnormalities. (Figure1.) There was no ST-segment changes concerning for ischemia.


Figure 1. Presenting ECG with initiation of transcutaneous pacing. The large voltages recorded on the right side of the ECG occurred when the transcutaneous pacing was started.


A limited transthoracic echocardiogram showed severe bradycardia in action, but the actual contractility was normal, and no focal wall motion abnormalities were identified. (Figure 2.)


Figure 2. Click here to see a limited transthoracic echocardiogram using the subcostal window.


A small pericardial effusion could be seen as the thin hypoechoic line starting anteriorly and wrapping around the apex to the posterior aspect. No echocardiographic evidence for tamponade was present based on the lack of right ventricle collapse during diastole.


Abdominal ultrasound was notable for a small amount of intraperitoneal free fluid, pleural effusions, and a dilated IVC with no respiratory variation. (Figures 3, 4, and 5.)


Figure 3 (left). Abdominal ultrasound in the hepatorenal (Morrison) window. A small amount of free fluid is visible in the potential space between the liver and kidney. Figure 4 (center). Right thoracic ultrasound showing pleural effusion. Lung parenchyma is usually anechoic, preventing visualization of the posterior lung bases. The lung base is clearly seen in this situation, however, and is hypoechoic, indicating a fluid-filled area consistent with pleural effusion. Figure 5 (right). Ultrasound view of the IVC. It is dilated, and there was no respiration variation. Click here to watch an ultrasound of this finding.


This was presumed to be volume overload from a combination of ascites given the patient’s history of cirrhosis and renal failure.


Initial laboratory tests showed normal blood counts and a chemistry panel that was notable for a potassium of 7.4 mEq/dl. Given the difficulty of achieving adequate transcutaneous pacing, a right internal jugular introducer sheath was inserted, and a transvenous pacing wire was placed with successful mechanical and electrical capture. (See Table 1 for how to place a transvenous pacemaker. Figure 6 shows the pacing wire within the right ventricle.)


Table 1. Abbreviated Procedural Steps for Transvenous Cardiac Pacing
1. The entire procedure should be done under sterile conditions with full barrier drapes.
2. The sterile sleeve should be placed on the pacer wire once the sheath introducer is placed.
3. Inflation of the floating balloon should be verified.
4. The proximal (+) lead should be on the positive terminal on the connector adaptor.
5. The distal (-) lead should be attached to lead V1 on the cardiac monitor using an alligator clip.
6. The balloon should be inflated after the pacing wire is threaded 15-20 cm to exit the end of the sheath.
7. Advance the pacing wire in a smooth fashion while monitoring the ECG. Marked ST-segment elevation will occur when the lead tip contacts the endocardium.
8. Secure the protective sleeve.
9. Detach the negative lead from the ECG, and connect it to the connector adaptor of the pulse generator.
10. Initial generator settings should be 80 beats/min, output 5mA, and sensitivity of 3 mV.
11. You should be able to note mechanical capture by noting cardiac contractility at the rate set on the pulse generator. This can be done by palpating a pulse or contractions over the anterior chest wall or by visualization using ultrasound.
12. Test electrical capture by challenging the required output threshold and sensitivity.
A. With sensitivity set to maximum, gradually reduce your output threshold until electrical capture is lost. Set the output threshold at 2-2.5 times the value at which capture was lost.
B. Set the rate at 10 beats/min above the intrinsic rhythm. Place the pacemaker in asynchronous mode and ensure complete capture.
C. Then with the sensitivity set at about 3 mA, decrease the rate until pacing ceases. Verify that the generator is indicating that a native beat is sensed on every cycle. If not, increase the sensitivity. Reduce the sensitivity if the pacer oversenses and is being triggered by p or T waves. Set the sensing level at half of the value once the sensing level is determined (i.e., reduce the sensitivity by half.)

Figure 6. Click here to see a cardiac ultrasound in subcostal window. Transvenous pacer wire can be visualized as the hyperechoic structure within the right ventricle.


A chest radiograph and ECG was not obtained in ED following placement of the transvenous pacemaker. The patient was admitted to the medical ICU and cardiology consultation was requested. Emergent hemodialysis was arranged with the nephrology service. Unfortunately, intermittent loss of capture started occurring during transport from the ED to the ICU and from the trolley to the bed. Within a short time, the transvenous pacemaker failed capture completely despite increasing the output and sensitivity settings on the pacemaker, and the patient returned to his native bradycardic rhythm. The admitting team obtained a chest radiograph. (Figure 7.)


Figure 7. AP chest radiograph after arrival in the ICU.


The endotracheal tube is in good position, and external pacer pads are over the left hemithorax. The pacer wire takes a crazy course, however. It can be seen entering from the top of the film through the right internal jugular vein and descending the SVC (right of midline) to the heart. It is coiled in the right ventricle, however, and part of the wire is likely looping through the tricuspid valve. The electrode tip appears to be abutting the high septal wall. A schematic is shown to help visualize the misplaced pacer wire. (Figure 8.)


Figure 8. Schematic of misplaced pacing wire.


A 12-lead ECG was obtained immediately after the pacer was placed. (Figure 9.) Pacer spikes appear prior to each QRS complex. The emergency physician interpreted this ECG as an indication of successful placement, which is why a chest x-ray was not immediately obtained. This is an abnormal ECG for a patient undergoing transvenous pacing, however. The QRS complex is narrow with an axis downward and to the left, indicating that the lead contact is atrial or high on the septal wall. A properly placed right ventricular lead placement in the apex should result in a LBBB and an upwards QRS complex. Capture was likely lost when the pacing tip was pushed out of the ventricle and was not in contact with the right atrium wall.


 Figure 9. ECG after transvenous pacer placed.


The patient was taken to the cardiac catheterization lab to reposition the pacing wire under fluoroscopy. The wire was confirmed to be coiled and almost tied in a knot. The tip was in the atria, and the floating balloon was partially inflated. It was repositioned without difficulty and achieved excellent capture. The patient was returned to the MICU, and ultimately underwent emergent dialysis to correct the underlying hyperkalemia.


Cardiac pacing can be a life-saving procedure, and the emergency physician should be ready to place a transvenous pacer if transvenous pacing is unsuccessful. Familiarity, practice, and checklists can dramatically increase the probability of success and enhance patient safety.

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Wednesday, October 01, 2014

Winning teams have depth, and games are often won from the bench or deep in the batting order. That is certainly true when competing against ventricular fibrillation, and a few tools you might not know can help these patients.


A 55-year-old man with severe coronary heart disease and previous four-vessel coronary artery bypass surgery collapsed at a mall. He also had an unprotected left main atherosclerotic plaque. Bystanders immediately began chest compressions, and the available AED, unfortunately, advised no shock.

Paramedics started bag-valve-mask ventilation and high-quality mechanical compressions with a Lucas device. The initial rhythm was ventricular fibrillation, and multiple defibrillation attempts were unsuccessful. Amiodarone and epinephrine were given, along with more shocks between high-quality chest compressions without success.


The patient was intubated, and ventilations were provided with the ResQPod impedance threshold device. ACLS-driven resuscitation continued in the ED with defibrillation and additional doses of amiodarone, lidocaine, magnesium, epinephrine, and vasopressin, all with no return of spontaneous circulation. Cardiac ultrasound showed no organized cardiac activity.


Ventricular fibrillation is a rapidly fatal rhythm. Patients have no organized electrical activity or cardiac output. VF is often precipitated by myocardial ischemia, and it never terminates spontaneously. It is often the initiating event of sudden cardiac death. Treatments for ventricular fibrillation are directed at restoring perfusion to ischemic myocardium, correcting oxygenation and ventilation deficits, stabilizing the myocardium, and correcting electrolyte abnormalities.


The patient received high-quality uninterrupted CPR, electrical defibrillations, vasopressors, and antiarrhythmics, but still had persistent VF. Now what?


Patients who suffer a cardiac arrest and attempted resuscitation have elevated catecholamines, and they can be markedly elevated for those who have been treated with epinephrine (often multiple times). Epinephrine is a nonselective adrenergic agonist, stimulating β1, β2, and α receptors. The increased contractility, heart rate, automaticity, and peripheral vasoconstriction increase the work, oxygen consumption, and irritability of already damaged myocardial cells. The use of β-adrenergic receptor blockers to counter the effects of epinephrine and endogenous catecholamines is an option. Animal, retrospective, and small prospective studies support this.


Early guidelines suggested propranolol after antiarrhythmics, but today esmolol is more effective. It provides short-acting β1-selective blockade, which allows it to exert its effect during the resuscitation with less long-term worsening of cardiogenic shock once spontaneous circulation is achieved.


Another option is high-energy defibrillation. Electricity works by depolarizing the myocardial cells and creating a zone of myocardium that has an extended refractory period. This zone stops the propagation of micro- and macro-reentrant activating circuits and wavelets. Atrial fibrillation and ventricular fibrillation are electrically stable rhythms, so larger proportions of the myocardium must be depolarized to terminate the rhythm.


Monophasic and biphasic are the most common waveform shapes used in external defibrillation. The polarity at each electrode in biphasic waveforms reverses part way through the defibrillation waveform. The use of a biphasic waveform in cardioversion and defibrillation increases defibrillation success by depolarizing more of the myocardium, and reduces the development of postshock arrhythmias. This is why biphasic waveforms have been universally adopted.


Similarly, using higher defibrillation voltages can also depolarize more of the myocardium. Original work on defibrillators did not find much more improvement in the defibrillation success rate above 200 J of biphasic energy, and patients had more postshock cardiogenic shock. But research now shows that using higher defibrillation voltages can be successful in refractory ventricular fibrillation when other treatments have failed. Described in animal models by Geddes in 1976 and Hoch in 1994, the use of up to 400 J on patients with refractory ventricular fibrillation during electrophysiology procedures restored regular rhythm.


Most defibrillators are limited to 200 J, so high-energy defibrillation is performed by attaching a second set of pads to a second defibrillator, allowing up to 400 J of biphasic energy to depolarize the myocardium. It is important to ensure that the vectors of both depolarization vectors pass through the heart. (Figure 1.) Both shock buttons are pressed as simultaneously as possible. The high energy increases the likelihood of successful defibrillation, and the severity of post-resuscitation myocardial dysfunction increases with the magnitude of electrical energy delivered by the shock.


Figure 1. Defibrillator pad placement for high-energy defibrillation.


A third option that might seem way out there is a stellate ganglion blockade. The stellate ganglion is part of the sympathetic chain formed by the inferior cervical and first thoracic ganglia. It provides sympathetic innervation to the upper extremities, head, neck, and, most importantly for us, the heart. Blocking this nerve prevents sympathetic further cardiac stimulation. The procedure is usually performed under fluoroscopy for reflex sympathetic dystrophy, but it may be attempted by ultrasound guidance during resuscitation efforts for refractory ventricular fibrillation. The ganglion is located along the anterior spine, and is accessible by a percutaneous approach through the anterior neck. (Figure 2.) There is a risk, however, of residual left ventricular dysfunction. The blockade does not alter the circulating catecholamines, and is certainly a fourth-line treatment. Full details of this procedure can be found at

Figure 2. Ultrasound-guided approach for a stellate ganglion blockade.

Tuesday, September 02, 2014

“Doc to the radio phone,” went the call over the PA. This is often just medics notifying about a diabetic refusing transport or stopping a futile code, though like most of emergency medicine, it can be anything.

Then we heard, “STEMI. Activating prehospital.”

EMS had been called to the house of a 54-year-old man. He had been experiencing chest pain on and off for several weeks. The most recent episode began about 30 minutes prior to ED arrival. He described 8/10 retrosternal pressure that radiated down his arms. He was tachypneic, but denied shortness of breath and was not hypoxic. Other vital signs were normal.

He was slightly nauseated, but had not vomited and was not diaphoretic. Paramedics treated the patient with sublingual nitroglycerin and aspirin, and obtained an ECG en route to the hospital. (Figure 1.)

Figure 1. Presenting 12-lead ECG.

The ECG showed sinus rhythm with a rate about 60 bpm. There is diffuse ST-segment elevation in V2-V5, II, III, and aVF, with reciprocal depression in aVL. Maximal ST-elevation is 3-4 mm in lead V3. As part of the effort to reduce door-to-balloon time, our paramedics can activate the cardiac catheterization lab based on the clinical history and a 12-lead ECG obtained in the field that indicates STEMI, which is what they had done.

Once in the ED, the patient was given an additional sublingual nitroglycerin for ongoing chest pain and clopidogrel 600 mg. While the cardiac catheterization lab was being prepared, an emergent directed transthoracic echocardiogram was performed, which showed moderately decreased left ventricular systolic function (EF 35%) with akinetic regional wall motion abnormality of the distal septum, anterior, apex, and inferior regions. The patient was taken to the cardiac catheterization lab for emergent angiography and PCI.

He was found to have a 100% occlusion in the mid-LAD (Figure 2) that was reduced to 0% (TIMI III flow, see Table 1) with thrombectomy and then placement of a drug-eluting stent (DES).

Figure 2.

Click here to watch a video demonstrating angiography of the left main, LAD, and coronary arteries showing a 100% occlusion in the mid-LAD.

A co-culprit lesion was identified in mid-RCA with 100% occlusion that was reduced to 0% (TIMI III) with stenting. (Figure 3.)

Figure 3.

Click here to watch a video demonstrating angiography of right coronary artery showing a 100% occlusion in the mid-RCA.

The patient vomited during the procedure, which likely included the clopidogrel. The patient was therefore loaded with heparin and treated with bivalirudin.
The patient is placed on a radiolucent moveable table. A gantry surrounds the patient, with the x-ray source underneath the patient table projecting the x-ray beam up through the patient to the image intensifier and camera, which is above the patient’s chest. (Figure 4.)

Figure 4. Position of patient and gantry in the cardiac catheterization lab.

The gantry can be pivoted so that the x-ray beam takes different angles through the patient. The position of the gantry is referenced with respect to the image intensifier/camera. Left anterior oblique (LAO) and right anterior oblique (RAO) images are obtained when the camera is pivoted toward the patient’s left and right sides, respectively. (Figure 5.)

Figure 5. Visualization of the RAO and LAO views as seen from the patient’s feet.

The camera is also able to pivot toward (cranial) and away (caudal) from the patients head. Controls allow the interventionalist to position the camera, raise and lower the table and the camera, change the magnification, open or close the collimator, activate fluoroscopy, and record cine, among others.

Under x-ray fluoroscopy, a catheter is guided through the aorta to the heart, and the tip is manipulated to engage the ostium of the coronary artery. Pressure is measured at the tip of the catheter. After engaging the ostium of the coronary artery, it is confirmed that the tip of the catheter is free, and not against the wall of the artery, under a subintimal plaque, deep into a small vessel, or mechanically obstructing an ostial or very proximal stenosis. This is accomplished by confirming that the pressure is not damped and with the use of a test injection using a small amount of contrast material.

Angiograms are obtained and recorded digitally (cineangiographic) while injecting an iodinated contrast material through the catheter (either by hand or power-injected) to opacify the coronary artery. Several cardiac cycles are recorded while the observing runoff of the contrast material through the distal coronary artery. Often, slight opacification of the coronary veins can be observed.
 The different coronary arteries can be visualized in various views or projections, which can be obtained by rotating the x-ray camera around the patient. (Figure 6.) By isolating the individual coronary arteries and imaging from multiple angles, luminal obstructions can be identified with increased accuracy and minimize the misinterpretations that can occur based on single two-dimensional projections.

Figure 6. Camera positioning for best coronary angiography views by selected coronary arteries.

The patient had persistent cardiac dysfunction following revascularization of the LAD and RCA coronary arteries. Left ventricular end-diastolic pressure (LVEDP) was 52 mm Hg, indicating significant impairment of systolic function and decreased compliance. He became hypotensive. An intraaortic balloon pump counterpulsation was placed for afterload reduction and increased coronary artery perfusion. Acute pulmonary edema and hypoxia developed, and the patient was emergently intubated. High FiO2 and PEEP improved his oxygenation. A bedside echocardiogram showed stunning of anterior and septal regions without thinning. The patient’s LVEDP decreased to 29 mm Hg following placement of the balloon pump and intubation.
Acute coronary artery occlusion, such as the patient experienced, causes myocardial hypoxia and ischemia and rapid depletion of ATP, which results in both systolic dysfunction (loss of inotropy) and diastolic dysfunction (impaired relaxation and reduced compliance). The dysfunction is reversible if coronary flow can be reestablished and perfusion restored, before myonecrosis occurs. The stunned myocardium exhibits prolonged postischemic dysfunction after the initial hyperemic phase of reperfusion, and is less responsive to inotropic drugs, which can result in cardiogenic shock. It can take hours to weeks for normal function to return.

The ischemic myocardial cells prioritize metabolic processes inside the cell over contractile function, however, if regions of myocardium are exposed to chronic ischemia. This is called myocardial hibernation. The myocardial cells remain viable, but chronic dysfunction occurs. Hibernating myocardium should be suspected when there is coronary artery disease and chronic ventricular dysfunction (regional wall motion abnormalities to ischemic cardiomyopathies). Assessment of viability can be performed with a dobutamine stress echocardiogram, thallium scintigraphy (SPECT), PET imaging, or cardiac MRI. For example, the contractility and regional wall motion abnormality will improve with administration of low-dose dobutamine, but at higher doses will generate inducible ischemia and increased dysfunction. This biphasic response is classic for hibernating myocardium. Successful revascularization will restore coronary flow and recovery of contractile function. Infarcted areas are often a mixture of scarred and hibernating tissue, even with transmural infarctions (Q-waves on ECG).

Intermittent short episodes of ischemia, such as in patients who experience chronic angina, can cause adaptation within the heart called preconditioning, which can protect the myocardium for subsequent damage from a larger ischemic insult. The mechanisms of stunning and hibernation are not completely understood, but evidence suggests that it is related to impaired Ca++ handling by the sarcoplasmic reticulum and because of damage caused by oxygen free radicals.

Reperfusion itself can contribute to impaired function, electrical disturbances, and infarct size. When oxygen is made available to the ischemic myocardial cells, there is a sudden burst of production of oxygen free radicals by neutrophils. This produces a chain reaction of radical species, which can damage cell membranes and impair cellular function. Additionally, this upregulates the inflammatory response, which can further damage tissues.

The patient did well, however. The inotropic support was no longer needed within several hours, and the IABP was removed within 24 hours. A repeat 12-lead ECG after reperfusion showed decreased ST-elevation in III and aVF with reciprocal depression in I and aVL. (Figure 7.) The anterior ST-elevation had resolved. There is late precordial R/S transition consistent with anteroseptal infarct. A repeat echocardiogram performed on day 3 of hospitalization prior to discharge showed resolution of wall motion abnormalities and an EF of 50%.

Figure 7. ECG obtained after reperfusion of LAD and RCA coronary arteries.


Tuesday, August 05, 2014
When a patient arrives to your ED fresh from karate class still in her uniform, you get a feeling about where the case is heading. This patient was 49, and reported that she always had some aches after karate. This evening, though, her pain was very different — and much more concerning. The pain had started about an hour into her class and worsened over the next 30 minutes. It was a severe achy pain over her left chest that radiated to her neck and was associated with pronounced diaphoresis. This prompted an expedited cardiac workup.
The ECG showed a sinus tachycardia with ST-elevation in V2-V3, I, aVR, aVL, with depression in II, III, aVF, and V5-V6. The ST-elevation in V2-V3 with inferior reciprocal depression (II, III, aVF) was concerning for myocardial injury in the anteroseptal region caused by left anterior descending artery (LAD) occlusion. EPs should have a high suspicion for very proximal LAD, left main, or Circumflex occlusion when seen in conjunction with ST-elevation in I, aVL, and aVR.
Figure 1.
She was taken immediately for coronary angiography, and was found to have an extensive thrombosis originating in the left main and extending into the proximal LAD and Circumflex arteries. The clot was removed by aspiration thrombectomy, and further angiography and intravascular ultrasound revealed dissection of the coronary arteries originating in the left main and propagating down the LAD. A small perforation of the LAD was seen just proximal to the first diagonal takeoff.
Figure 2.
Spontaneous coronary artery dissection (SCAD) is an uncommon event, and occurs when the layers of the artery separate, creating a false lumen. Hemorrhage into the false lumen propagates the dissection distally. The true lumen of the vessel can become blocked by thrombus or the dissection flap. Obstruction of the lumen reduces perfusion and causes myocardial ischemia and necrosis. Patients present with symptoms of ischemic cardiac chest pain and with associated ECG and enzyme changes typical of NSTEMI or STEMI. ACS is often the initial concern, but the diagnosis of SCAD is made during coronary angiography.
The dissected medial flap shows up as a thin radiolucent line. Overlying thrombus is seen as haziness in the true lumen. SCAD is often treated with percutaneous intervention. Using IVUS, the dissection flap can be identified, and a guide wire can be placed carefully in the true lumen. Stenting open the flap seals the dissection, preventing further propagation, restoring flow in the true lumen, and relieving ischemia. Coronary artery bypass surgery is often difficult. Grafting to the true lumen is difficult with long dissections, and the vascular tissue is often too fragile to support suturing.
Atherosclerotic plaque rupture can cause complex intramural hematoma formation in the vascular wall dissecting the layers, but the dissection rarely propagates much further than the extent of the atheroma. More commonly, though, dissection associated with atherosclerotic plaque rupture can occur during balloon angioplasty or PCI. As the vessel is dilated, the fibrous cap and intimal layer can be torn, leading to dissection. Dissection in these scenarios is not usually labeled SCAD.
SCAD, in contrast, is not associated with coronary artery disease. Women make up the majority of cases, and they tend to be younger. A significant percentage occurs in the peripartum period, and the LAD is the most affected coronary artery. SCAD has also been associated with Marfan syndrome, fibromuscular dysplasia, and peripheral eosinophilia disease.
Figure 3.
Unfortunately for our patient, she had profound cardiogenic shock and was emergently placed on VA ECMO (which I will cover in the future) despite thrombectomy and stenting of the dissection flap. She had little recovery of her cardiac function over the next two weeks, and was transitioned to a left ventricular assist device (LVAD) as destination therapy.
LVADs provide mechanical pump support for patients with severe heart failure as permanent treatment or a bridge to therapy. The most common device used today is the HeartMate II (Thoratec). It uses a continuous flow axial pump that is implanted in the abdominal wall. The inflow cannula (relative to the pump) draws blood from the apex of the left ventricle, and the blood is pumped through the outflow cannula into the proximal ascending aorta.
Figure 4.
(New Engl J Med 2007;357[9]:885.)
The pump is powered and controlled by an external controller and batteries that are connected to the implanted pump by a driveline. Important parameters reported by the LVAD are pump speed (RPM), power, pulsatility index, and flow estimate.
Patients with LVADs can present to the emergency department for any condition. The most important rule for evaluating a patient with an LVAD is to assess the patient as you would normally, completely independent of the device. Specific assessment of the LVAD itself is shown in Table 1, and common LVAD complications are listed in Table 2.

The patient did well, and she was discharged home after several more weeks in the hospital. She maintains close follow-up in the LVAD clinic and close contact with her LVAD coordinator. She is being evaluated for an underlying connective disorder.
About the Author

Charles Bruen, MD

Charles Bruen, MD, is a fellow in critical care medicine and emergency cardiology at Hennepin County Medical Center in Minneapolis. He has special interest in stabilization, resuscitation, hemodynamic evaluation, and emergency cardiovascular care. He obtained his undergraduate degree in aerospace engineering at the Massachusetts Institute of Technology, and worked in aerospace for several years, leading the effort at Beal Aerospace Technologies to develop the largest rocket engine since the Apollo program. He earned his medical degree at the University of Texas Southwestern Medical School at Dallas, and completed a combined residency in emergency medicine and internal medicine at Hennepin. Visit his website,, and follow him on Twitter: @resusreview.

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