The man is 38, with a respiratory rate of 40. He can only get two or three words out between breaths. The cardiovascular system equally strained, it requires a heart rate of 140 to maintain a mean arterial pressure of 80.
He has been feeling short of breath for months now, but it grew worse over the past couple of days. He is afebrile, has no pain anywhere, and nothing hurts. No trauma. No chills. Just a non-productive cough.
Look. Moderate work of breathing alongside the cough. Thoracic cage being pulled up instead of out. Pulmonary compliance must be low. The problem is either parenchymal or pleural.
This degree of tachypnea without work of breathing would indicate a non-parenchymal etiology: compensation for a severe metabolic acidosis or inadequacy of a large sector of his pulmonary vascular bed.
Listen. Decreased breath sounds throughout the left lower lobe, left lingular area, and left upper lobe. Is the entire area collapsed? His trachea is not shifted ipsilaterally to indicate loss of volume.
Is this a large pleural effusion? Trachea not shifted contralaterally either. Heart sounds are in the appropriate place, not displaced over the sternum or in the right hemithorax.
E or A? He has E to A changes in the areas of decreased breath sounds. It indicates something solid, or semi-solid, in direct contact with his tracheobronchial tree. Not often from a pleural effusion or collapse, E to A is usually consolidation. Every alveolus in the designated lung segments filled with something: transudate, exudate, pus, or blood.
Unlike collapse, which points to an upstream obstruction of bronchioles or segmental bronchi resulting in a loss of volume from negative pressure downstream; consolidation is a filling process. It is a positive, not negative, phenomenon. It is an alveolar, not an airway, problem.
Saturation is 92% on room air. Can he be this tachypneic and have this degree of consolidation with only a mild amount of hypoxemia?
Ratios. It depends on blood flow. If perfusion to his consolidated segments is as poor (or poorer) than ventilation, he can retain a respectable ratio of V to Q and avoid hypoxemia. With few RBCs heading to consolidated lung, they are easier to oxygenate. The ratio is deceiving. Normal ratios make us believe patients are faring adequately, but such percentages may just indicate horrible ventilation coupled with equally disappointing perfusion. As it turns out, hypoxemia is not a sensitive indicator of pulmonary disease.
PMhx. He has a history of diffuse large B-cell lymphoma on R-CHOP therapy, and just completed a fifth cycle. His wife says his tumor burden is mostly comprised of an anterior mediastinal mass.
So this is it. The solid structure causing E to A changes throughout his left hemithorax and anterior chest is cancer abutting his major airways, not consolidated alveolar space.
I look down at the electrocardiogram in my hands. It still doesn't make sense.
Do you have any pain?
How about pressure, tightness, soreness?
Nothing in your chest? What about your shoulder, arm, jaw?
At this point, I'll even take “burning,” a toothache, or some disconcerting belching.
I look back down at the cardiogram in my hands. They are still there: tombstone elevations in 1, avl, and V2–6 with deep depressions in 3 and avf. They did not go away upon hearing he had no symptoms.
They are objective data. They do not bow to symptoms, and they do not bow to our expectations or desires for the case to make sense. Doggedly pursued by hard data, we are forced to conform and, at times, abandon the subjective.
I need more. Rather than being hunted by the objective, I choose to hunt it.
“Can you pull up his old records?” A few clicks later, and my resident has the bedside computer displaying a CT scan from one month ago.
He has a large anterior mediastinal mass filling the retrosternal space and enveloping the superior vena cava and the pulmonic and aortic roots. Squirming through the mass, filled with a sliver of contrast, I see it.
The left coronary artery. Main, anterior descending, circumflex, all fighting their way through a heavy burden of encasing tumor. Disrespectful B cells eroding their way through the pericardium now sit up against the lateral wall of the left ventricle.
Classic ACS? He is 38, and his left coronary artery may not have ruptured atheroma. Instead, the poor vessel could be choking. Strangulated on all sides, compressed and smashed. The tumor had responded to R-CHOP and was apparently shrinking one month ago, but today is a different story. The vise on the tributaries of the left coronary could be tighter. A large anterolateral STEMI from extrinsic compression of a coronary vessel?
Or has the tumor eroded its way into the epicardium itself? The two are confluent by CT, and we lack the detail to tell anything more. What we could be looking at are aberrant repolarization patterns from disrupted myocytes not because of upstream ischemia but rather direct invasion.
And the absence of pain? I postulate it is because of a neuropathy. Not one of somatic nerves in the extremities, like a diabetic or alcoholic who can no longer feel the soles of his feet, but rather a visceral neuropathy. Not metabolic from subpar axonal transport of nutrients or nonenzymatic glycosylation of distal nerve fibers or inadequacy of the small vasonervorum. Instead I believe it to be from encasement of visceral afferents in the anterior mediastinum. All the nerves that modulate his sensation of myocardial distress are living under the reign of a large, aggressive B-cell tumor. It has no regard for their well-being. Like the deinnervated cardiac transplant recipient, he may not be capable of feeling myocardial pain.
What can we do? He has plenty of muscle at risk, enough that his contractility has dropped to the point of doubling his heart rate to maintain a normal brachial artery tone. He is young, and the tumor is reportedly responding. The chemotherapy needs time. But right now, at this moment in the night, chemo or radiation are not practical ways to release the vise. Our only chance may be to have the interventionalist stent a coronary in the face of external invasion.
The zebra. The left main and circumflex are patent, and a 99% proximal lesion of OM1 is stented in the catheterization suite. Beyond that, a vise is suspected as the vessel abruptly terminates. A stent restored TIMI III flow up to this point, but nothing can be done for the distal compression.
Post-procedure electrocardiograms revealed the same diffuse tombstone pattern. And his troponin would only peak at 1. Why the persistent large territory of anterior-lateral ST elevations in the face of a meager troponin rise and a patent left main, anterior descending, and circumflex? I have to say for this unfortunate 38-year-young man, the initial possibility of direct myocardial invasion by tumor has become a grim probability.
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