UMEM Educational Pearls - Cardiology

The standard dose for adenosine in treating SVT is 6 mg given as a rapid IV push. The dose should be immediately followed by a saline flush and works best if the drug is administered through a good, proximal (e.g. antecubital) IV line.

A few points:

1. The initial dose of adenosine should be reduced to 3 mg if the dose is administered through a central line, if the patient has a transplanted heart, or if the patient is taking carbamazepine or dipyridimole.
2. The initial dose of adenosine should be increased to 9-12 mg if the patient is taking theophylline or large doses of caffeine.
3. ALWAYS warn the patient that he/she will experience 5-10 seconds of chest pressure, warmth, dyspnea, and perhaps a feeling of "impending doom" as the adenosine kicks-in, and reassure the patient that the sensation will resolve. Failure to warn the patient of these symptoms may result in the patient refusing to ever take the medication again...plus it's just plain cruel to not warn the patient.

A few pearls regarding pacing a patient with an unstable bradycardia:

If the patient has an implanted pacemaker (which isn't working properly), the transcutaneous pacing pads should be placed at least 10 cm away from the implanted PM pulse generator.

Placement of a transvenous pacemaker is absolutely contraindicated if the patient has a prosthetic tricuspid valve.

Neither transcutaneous or transvenos pacing is likely to work in the setting of severe acidosis or severe hypothermia. Severely hypothermic patients, in fact, have very irritible myocardial tissue and therefore attempts at pacing may produce ventricular dysrhythmias.

Atypical presentations of ACS in the elderly are common.
Only 40% of patients > 85yo present with chest pain. Dyspnea is the most common presenting complaint in these patients. Other atypical presentations include isolated nausea, vomiting, diaphoresis, or syncope.

The presence of an atypical presentation is not reassuring in terms of prognosis. Patients presenting atypically have a 3-fold higher in-hospital mortality (13% vs. 4%). This doesn't even include the patients that are inadvertently discharged home because of failure to diagnose ACS.

Although CHF is usually associated with low cardiac output, "high output failure" can occur as well. In this condition, cardiac output is normal or even high but not high enough to meet markedly elevated metabolic demands of the heart in certain conditions. Those conditions include: severe anemia, thyrotoxicosis, lartge arteriovenous sunts, Beriberi, and Paget disease of the bone.

 

The T-wave in lead V1 is usually inverted or flat. When the T-wave is upright, especially if it is tall (taller than the T-wave in lead V6), be worried about cardiac ischemia...especially if the large upright T-wave is a new finding compared to prior ECGs.

LVH, LBBB, and misplaced precordial leads are the other causes of tall upright T-waves in lead V1. In the absence of any of these three conditions, worry about ischemia.

Marriott described this finding many years ago and refers to it as "loss of precordial T-wave balance."

Recent  studies have identified that a significant cause of morbidity and mortality in women, elderly, and patients with renal failure is the failure to consider renal insufficiency in dosing certain anticoagulants and anti-platelet medications, resulting in bleeding complications. Medications should be based on creatinine clearance, NOT SERUM CREATININE. When the creatinine clearance is < 30 mL/min, the dose of any renally-excreted medications should be decreased.

For example, an 85 yo woman that is 110 lbs and has a serum creatinine of 1.2 (sounds normal!) actually has a creatinine clearance < 30, which means that she has relative renal insufficiency. Her dosages of medications (e.g. enoxaparin) should be adjusted for this.

 Creatinine clearance can easily be calculated via computer programs that you can "google" (e.g. just google "creatinine clearance calculation"). If you enter the patient's gender, age, weight, and serum creatinine, the programs will calculate the value for you.

New onset atrial fibrillation is rarely the sole manifestation of myocardial infarction. In other words, in the absence of accompanying chest pressure, dyspnea, diaphoresis, or other anginal equivalents, a rule-out ACS workup in not supported by the literature and is not cost-effective.

The two exceptions to the statement above are elderly and diabetic patients, in whom subtle presentations of ACS are common with or without atrial fibrillation.

In the treatment of an acute ST-elevation MI, there are three major signs of successful reperfusion:

1. T-wave inversion within the first 4 hours. If the T-wave inversions occur beyond 4 hours, it's uncertain.
2. Resolution of the STE by at least 70% in the lead with maximal STE.
3. Development of a "reperfusion arrhythmia," most notably accelerated idioventricular rhythm (AIVR), which looks like V.Tach but the rate is only 60-120. Remember, V.Tach should have a rate > 120.

Persistent pain/symptoms OR absence of STE resolution by 90 minutes warrants strong consideration of rescue angioplasty.

Hypertrophic cardiomyopathy is associated with a systolic murmur loudest at the apex, and it may radiate to the base. The murmur increases with maneuvers that cause ventricular filling to decrease (e.g. valsalva, standing). The murmur decreases with maneuvers that cause ventricular filling to increase (e.g. trendelenburg, isometric exercises, squatting). These patients have primarily diastolic dysfunction, and so they should be treated with beta blockers to help improve diastolic filling time.

The consequences of missed MI in the elderly are dramatic: 50% of elderly patients with an MI missed by the ED or primary care doctor will be dead within 3 days.

Acute pericarditis Up to 60% of patients with acute pericarditis are asssociated with a pericardial effusion. Grading of the effusion is as follows:

• "Small" = less than 10 mm of echo-free space (anterior plus posterior)
• "Moderate" = 10-20 mm
• "Severe" = > 20 mm.

Ideally, the effusion echo-free space is measured at the onset of the QRS complex in diastole. Small effusions do not mandate admission in and of themselves. Severe effusions mandate admission. For moderate effusions, it's a judgement call and probably depends on how good the follow up is and also the patient's symptoms.

Mitral valve prolapse is one of the most common valvulopathies and, although usually benign, it can predispose to atrial dysrhythmias, bacterial endocarditis with systemic embolization, and sudden death. If these patients have an audible murmur (as opposed to just the click), it implies that there is regurtitant flow and these patients are then generally considered candidates for bacterial endocarditis before procedures which can induce bacteremia. This includes dental extraction!

Fondaparinux is a selective factor Xa inhibitor. Benefits of fodaparinux vs. heparin when anticoagulants are used in ACS: 1. It is not associated with heparin induced thrombocytopenia. 2. Significant reduction in 30-day and 6-month mortality vs. enoxaparin. 3. Significant reduction in bleeding complications. 4. Safer in patients with renal insufficiency vs. enoxaparin. Unfractionated heparin should be continued while the patient goes for PCI.

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.

Thanks again to Larry Weiss, MD, JD Disclaimer: This information does not constitute legal advice, is general in nature, and because individual circumstances differ it should not be interpreted as legal advice. The speaker provides this information only for Continuing Medical Education purposes.

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).

Post-MI patient develops acute pulmonary edema + hypotension + new systolic murmur = VSD or paplillary muscle rupture Treatment = inotropic support + afterload reduction (as tolerated) + OR ASAP (balloon pump is temporizing)

--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