Brit: Thanks for joining us on the emDocs.net podcast. I’m Brit Long, and I’m joined by Manny Singh. We have 4 great posts to talk about. The first one is Diagnosing Cardiogenic Shock, published on Monday, February 3. This post looks at the diagnosis of cardiogenic shock based on history, exam, labs, and imaging. Manny, why is this post important?
Manny: This is such an important condition to diagnose as quickly as we can. The key points for your next shift is that CS is primarily caused by an acute MI (~70% of cases) and is the focus of most studies, but other causes should also be considered. Other causes are shown in Table 1 of the post but include myocarditis, cardiomyopathy, aortic insufficiency and many others. Mortality is pretty severe, around 60%. History and exam should focus on evaluating for hypoperfusion and pulmonary congestion, and then quickly addressing them. JVP is an important physical exam component for the diagnosis of CS and is associated with increased mortality. US is super helpful, with a RUSH exam having a sensitivity and specificity 89% and 97%. If you’re an ultrasound jedi, calculations of EF, CO and CI through LVOT VTI is the next level. Figure 5 in this post gives a great summary and algorithm that I’ve used to review with my residents.
Brit, let's briefly review how we manage these CS once we hone in on the diagnosis? What's your pathway?
Brit: First, get a 12-lead ECG while ABCs are being evaluated. As you mentioned, an AMI not is the major cause of cardiogenic shock but is also rapidly treatable. These patients usually will not have subtle acute myocardial infarction. They’ll typically have large anterior STEMIs although inferior STEMI with extension into the RV is also common. Don’t forget to look closely for elevations in aVR, which represent significant left main coronary artery (LMCA) or left anterior descending (LAD) artery disease. Once a STEMI is identified, get your cath team on the phone immediately. Opening of the culprit vessel is the intervention most likely to save the patient. Unfortunately, thrombolytics are not very effective in STEMI with cardiogenic shock. These patients have intense thrombolytic resistance likely secondary to marginal drug delivery (secondary to low diastolic pressure and thus low coronary artery filling pressures as well as acidosis). The SHOCK registry found that thrombolytics did not significantly change mortality.
How do we go about managing their airway if needed?
Manny: Excellent question! Patients with cardiogenic shock will have severe respiratory distress. Unlike patients with ADHF, they often will not tolerate non-invasive positive pressure ventilation (NIPPV) and will require emergent intubation. Unfortunately, these patients are challenging to intubate as they have all three of the “HOp killers” (hypotension, hypoxia and acidosis) as discussed by Scott Weingart. The big critical pieces are maximizing pre-intubation hemodynamics (small fluid bolus, push dose pressors, or IV pressor) and pre-oxygenation with head up position as well as continuing oxygenation during intubation with apneic oxygenation. All this helps in successfully intubating your patients with longest possible safe apnea time.
Brit, how do you address perfusion of these patients?
Brit: While addressing airway, breathing and getting an ECG to aid with diagnosis, you have to address circulation And improve perfusion to the brain and coronary vessels. vasoactive medications. The optimal agent would be one that increased coronary artery perfusion, had minimal effects on heart rate, decreased afterload and decreased myocardial oxygen demand while enhancing cerebral perfusion pressure. Unfortunately, no such agent exists.
Manny: The gut instinct of many physicians is to reach for an inotrope like dobutamine. However, caution must be practiced here. Dobutamine has beta-1 and beta-2 agonist activity, which may augment cardiac output but will also cause vasodilation. The balance between increased output and peripheral vasodilation leads to the classic teaching that one-third of patients will drop their blood pressure, one third will have no change in blood pressure and one-third will have increased blood pressure. Unfortunately, there’s no good way to predict which patient will have which response. This can be combated by initiating a vasopressor first and then adding the inotrope when blood pressure has become relatively stable (shooting for a MAP = 65 mm Hg). There is no optimal vasopressor for this indication.
The ACC/AHA recommends the following (Overgaard 2008):
SBP 70-100 (w/o signs of shock) Start dobutamine
SBP 70-100 (w/ signs of shock) Start dopamine
SBP < 70 Start norepinephrine
Brit: I think a lot of physicians have issues with dopamine. I really like norepinephine as a first line pressor in this situation. An RCT of patients with undifferentiated shock showed that norepinephrine was superior to dopamine specifically in the subgroup of patients with cardiogenic shock (De Backer 2010). Although it’s recommended that norepinephrine be given through a central line,you can use a good peripheral line while central access is being obtained. Epinephrine (adrenaline) is a viable alternate option as well as it may increase cardiac contractility as well as increasing MAP.
Manny, is there a role for intra-aortic balloon pumps (IABP) in these patients?
Manny: In theory, IABP placement makes sense. It should increase myocardial oxygen supply by increasing coronary artery perfusion and decreasing myocardial oxygen demand. The largest study of IABP in cardiogenic shock was published in the NEJM in 2012. In this prospective, randomized, unblinded (hard to blind a patient or doctor to the presence or absence of a large catheter in the groin) trial, the authors demonstrated no mortality benefit to IABP placement (Thiele 2012). This trial had many flaws but challenges the potential benefits of IABP placement.
Brit: Our next post released on February 17 looks at prostatitis. Prostatitis is an acute or chronic infection of the prostate. The key to diagnosis is considering the disease. Patients with recent urologic instrumentation, immunocompromise, diabetes or anatomic abnormalities are at higher risk for prostatitis. While e. Coli is the most common microbe involved, keep in mind Chlamydia and Gonorrhea in sexually active patients. Patients with acute prostatitis may have systemic signs of infection, back pain, and abdominal pain. The prostate is usually tender, edematous and boggy on digital rectal exam, with a sensitivity of 63.3% and specificity of 77.7%.Other sources report more than 95% of patients have prostate tenderness on exam. Urinalysis is often relied upon for diagnosis. However, prostatitis is a clinical diagnosis! UA and urine culture may be negative, so be sure to consider the bigger clinical picture. Treatment includes antibiotics, typically for an extended period of time. Patients with sepsis, poor follow-up, acute urinary retention, or concern for other infections such as endocarditis should be admitted. Complications can be severe, including prostatic abscess. CT imaging can be used to evaluate for prostatic abscess, which should be considered in patients who do not symptomatically improve with antibiotic treatment. I recommend looking at the post for antibiotic recommendations, but a longer course is recommended compared to your standard UTI therapy with outpatient followup.
Manny: Our ECG Pointers post by Lloyd Tannenbaum from your shop looked at stent thrombosis. These are important to consider when a patient presents after a PCI with an identical EKG distribution of their prior MI. When PCI is done with a bare metal stent, approximately 25% can be completely occluded at 14 days post PCI. And this is despite high doses of heparin and other antithrombotic medications.
There were several strategies attempted to decrease thrombosis including using high pressure balloon expandable stents and heparin impregnated stents. They were able to decrease the rates of occlusion to around 3%, but with increasing doses of antithrombotic medications, rates of hemorrhagic complications increased from 3-4% to 7-13%. Luckily in the early 1990s, several studies looked at combining aspirin and ticlopidine, and from those studies, dual antiplatelet therapy was born and a game changer.
Current stents are drug eluting stents, which are stents that send out (or elute) drugs that prevent inflammation and scar tissue in the coronary vessels. This helps to prevent stent thrombosis and failure. Interest ingly, current stents can even be bioresorbable, where over time, the body will completely reabsorb the stent. Currently, using dual antiplatelet therapy and modern stents, the rate of stent thrombosis, 9-12 months after stent placement is 0.61%
Brit: Our final post from the Unlocking Common ED Procedures series looks at central venous catheter placement. The great thing about this post is it has a downloadable pdf you can use for quick reference. When it comes to selecting a site for placement, there is no single best access site for a central venous catheter and you might find yourself in situations where any of the 3 sites may be necessary. Subclavian access has an overall lower rate of infection and thrombosis with an increased risk of pneumothorax. Subclavian access may be preferable in the setting of blunt and/or penetrating thoraco-abdomino-pelvic trauma if there is concern for vascular injury at or above the femoral vein and the internal jugular vein is inaccessible due to cervical spine precautions. Femoral access was initially thought to have a higher infection rate with the advantages of being distant from the thorax and an easy site of compression if a hematoma develops. However, more recent data suggests there is no increased risk in catheter-related infections with femoral access, compared with other sites. It may also be the correct choice in patients with suspected coagulopathy. Internal jugular access has a relatively low risk of infection as well as iatrogenic pneumothorax under ultrasound guidance. Thus in critically-ill patients who are not imminently dying, ultrasound-guided internal jugular access is often the preferred site of entry.
When placing, always keep the tip of the needle in view under ultrasound when advancing in order to avoid injury to underlying anatomic structures. Once the needle is within the vein and flow is obtained into the syringe, decrease the angle and recheck flow to assure the needle is still within the vessel. Brisk, even near pulsatile blood flow, can be seen when placing an internal jugular vein central line in the setting of certain pathologies such as heart failure or cardiogenic shock due to a severely elevated central venous pressure. In this situation, careful confirmation of the wire within the jugular vein should be performed with ultrasound. If resistance is felt while advancing the wire, cease advancement, decrease the needle angle and reattempt. If there is still resistance, remove the wire and reassess flow with the syringe. The emergency department can be a difficult place to maintain sterility. If there is any concern regarding the sterility of the central line, it is prudent to inform the admitting team for follow up care.
Manny: That rounds out our summary of the key emDocs posts. Thanks for joining us on our podcast, and stay tuned for our next episode where we talk about SJS and TEN, the 5 minute rapid neuro hand exam, and penile injuries. Feel free to comment on our site and let us know if you have any feedback. Stay safe and healthy everyone!