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Acute Coronary Syndrome (our number one area of liability) [Part 2]
- Describing the character of the pain is the most common element of the history (Braunwald and Lee & Goldman).
- The history is the threshold issue and determines whether the patient enters risk stratification (Braunwald).
- The most atypical features of chest pain are sharp, pleuritic and positional pain.
- One-third of all patients with an MI have no chest pain.
- One set of cardiac enzymes violates a strong national standard of practice.
- Serial enzymes do not rule out unstable angina.
- If discharging a patient, document why you felt the patient did not have ACS.
- The plaintiff attorney literature advises litigators to focus on the history.
The 2007 ACC/AHA Guidelines for management of patients with unstable angina and non-STEMI were just released. They once again suggest the use of abciximab (Reopro) as the preferred glycoprotein receptor antagonist in patients that are going for PCI. If there is an anticipated delay to PCI, then eptifibatide (Integrilin) or tirofiban (Aggrastat) are preferred. The best evidence for these medications is in patients being managed invasively rather than just medically.
The presence of "classic" cardiac risk factors (i.e. risk factors identified in the Framingham studies) is most useful for predicting the long-term risk of developing CAD, but they have limited utility at ruling out acute coronary syndrome. A recent study (ref below) from the CRUSADE registry (multicenter registry including tens of thousands of patients with ACS), for example, demonstrated that 10.5% of patients with proven non-STE MI had NONE of the traditional cardiac risk factors. NEVER rule out ACS just because a patient has few or no cardiac risk factors. The decision to admit and risk stratify patients should always be based on your HPI (OLDCAAR). [Roe MT, Halabi AR, Mehta RH, et al. Documented traditional cardiovascular risk factors and mortality in non-ST-segment elevation myocardial infarction. Am Heart J 2007;153:507-514.]
Times when amiodarone should be avoided in wide complex tachycardias: 1. prolonged QT or torsade de pointes -- amiodarone prolongs QT and may induce torsade or cause torsade to become intractable 2. pregnancy -- amio is the only class D antiarrhythmic...use anything else, even electricity! 3. rapid Afib with WPW -- the only published literature says this causes hemodynamic deterioration 4. AIVR -- turns it into asystole...a clean kill! 5. pseudo-VTach caused by hyperK, TCAs, and similar meds -- these are actually not VT but just wide complex tachycardias (that look like VT) caused by poisoned sodium channels...amiodarone further blocks the sodium channels and can cause asystole 6. pulseless VT or VFib cardiac arrest -- you won't actually make the patient worse, but the ONLY evidence indicates that all amio does is increase survival to ICU without improved mental status and without increasing survival to discharge...so essentially you take up more ICU beds and increase costs
The risk of bleeding complications related to enoxaparin increases in patients with renal insufficiency. In fact, many recommend that unfractionated heparin be used instead of low molecular weight heparin in these patients because there is more safety data regarding unfractionated heparin. If enoxaparin is used, the dose should be cut in half (or given only once per day instead of every 12 hours) when the GFR is < 30 mL/min (GFR can be easily calculated by google-able GFR calculators on the internet).
--50% of all STEMI patients have elevated admission glucose levels (>140 mg/dL) --hyperglycemia at the time of admission is an independent risk factor for in-hospital and 1-year mortality in patients wih STEMI --hyperglycemia induces reduced microvascular perfusion and has adverse effects on platelet function, fibrinolysis, and coagulation --tight control of glucose levels during and after STEMI is recommended by the ACC/AHA guidelines and appears to lower acute and 1-year mortality rates
-Most patients with acute pericarditis are effectively treated with high-dose aspirin or NSAIDS + colchicine - Aspirin dose: 2-4 gms/day - Colchicine dose: 1-2 mg for first day, then 0.5-1 mg/day for 3 months - The use of steroids in first-time acute pericarditis should be avoided, as it has been found to increase the chances of recurrence
The most common valvulopathy after blunt chest trauma is acute aortic insufficiency. These patients will present with a new diastolic murmur. Stability depends on the degree of AI. On the other hand, if a chest trauma patient presents with a new systolic murmur, think about acute septal rupture. These patients are much more often unstable, or may die before arrival. These diagnoses may be missed in the unstable patient because physicians focus on the abdomen in the unstable patient. Pay attention to the heart sounds also!
Calcium's main effect on the ECG appears to be on the duration of the ST segment, such that: 1. Hypercalcemia shortens the ST segment, producing also a short QTc. 2. Hypocalcemia prolongs the ST segment, producing also a long QTc. As an aside, there are only three conditions in which a short QTc is typically noted: hypercalcemia, digitalis toxicity, and a recently described syndrome that causes sudden death--"the short QT syndrome" (in which the QTc may be < 300ms...that's REALLY short!). As another aside, there are only two conditions that prolong the QTc via prolongation of the ST segment--hypocalcemia and hypothermia.
Acute Pericarditis Viral and idiopathic causes account for 80-90% of cases of acute pericarditis (AP) in immunocompetent patients from developed countries. Therefore empiric treatment and extensive search for an underlying cause is unnecessary in the majority of cases we see. However, the etiology of AP in developing countries is very different, with TB-related AP predominating. 70-80% of cases from Sub-Saharan Africa and more than 90% of HIV-related cases of AP are tuberculous. Therefore, in the U.S. tuberculous pericarditis should be strongly considered among immigrants/visitors from developing countries and among patients with HIV.
Rapid Atrial Fibrillation Treatment 50% of patients with new AF spontaneously convert within 48 hours AF > 48 hours --> chances of spontaneous conversion decreases and chance of embolization increases significantly Most EM texts and lecturers still recommend diltiazem as first line medication for early rate control Patients in whom beta blockers are preferred: AMI, thyrotoxicosis, or if patient is already on BBs NEVER combine IV beta blockers and IV calcium channel blockers --> synergistic effect will cause hemodynamic compromise; start with one type of medication and stay with it
GI Bleed and Myocardial Ischemia Myocardial ischemia or infarction occurs in up to 20% of patients with significant UGI bleeds. For reasons that are uncertain, the majority of these patients have "silent" MIs (i.e. no pain). It's also unclear whether these patients develop MI purely because of hypoperfusion or because the stress causes a plaque to rupture and thrombose. Whenever you have a patient with a massive UGIB, get an ECG early, regardless of whether or not the patient is having chest pain, and if it's concerning, get cardiology involved early as well. anecdote--I've seen 2 patients with STEMI in the presence of an UGIB, one at Mercy and one at UMMS; neither had chest pain; both got transfused, seen by GI, and went cath within several hours; the takeaway--get both consultants involved EARLY!
Ventricular dysrhythmias in pregnancy Amiodarone should be considered a last choice in pregnancy. It is the only class D antiarrhythmic, and even short infusions can be associated with fetal hypothyroidism, IUGR, fetal bradycardia, and prematurity. Lidocaine or procainamide are preferred. Also, cardioversion/defibrillation/pacing is considered safe in any stage of pregnancy.
Non-ACS causes of elevation troponins: 1. acute PE 2. Stanford A aortic dissections 3. acute heart failure 4. strenuous exercise (e.g ultra-endurance activities) 5. cardiac toxins 6. ablation therapy/cardiversion 7. cardiac infiltrative diseases 8. post-heart transplant (may persist up to 3 mos) 9. cardiac contusion 10. sepsis 11. rhabdomyolysis
AMI versus Aneurysm For ECG distinction between AMI versus ventricular aneurysm, look for reciprocal changes and height of T-waves: 1. Reciprocal ST depression strongly favors AMI. 2. Large T-waves in leads with Q waves and STE is likely AMI. Ventricular aneurysm usually gives you "blunted" or flat T-waves in those leads.
Syncope Patients with syncope that are considered to be relatively low risk for complications clinically (i.e. those patients that are not clear-cut admissions) should be evaluated for the 5 CHESS criteria (from the San Francisco Syncope Rules). If they meet none of those criteria, then they are considered to be at very low risk for short-term adverse outcomes and they can be discharged for outpatient follow-up. If they do have any CHESS criteria, they are considered to be at higher risk and admission should be strongly considered. CHESS criteria: history of CHF, hematocrit < 30, ECG abnormalities, shortness of breath, presenting systolic pressure < 90.
After the age 35, cardiac output decreases by approximately 1% per year. That means that elderly patients are at much higher risk for CHF, especially when they are stressed in some way. CHF can develop in the elderly as a result of any stype of infection or other non-cardiac insult. If decompensated CHF is diagnosed in an elderly patient, don't forget to evaluate the patient carefully for potential non-cardiac causes.