22: Electrocardiography

Published on 06/02/2015 by admin

Filed under Anesthesiology

Last modified 06/02/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1001 times

CHAPTER 22 Electrocardiography

William A. Baker, MD, Christopher M. Lowery, MD

1 Are all abnormal ECGs indicative of heart disease?

No. Just as some individuals are very tall, some individuals without real cardiac pathology have electrocardiogram (ECG) findings that deviate enough from the population mean to raise the question of heart disease. Careful history and physical examination may help identify individuals who truly have cardiac pathology. Noninvasive techniques such as echocardiography and cardiac magnetic resonance imaging may aid in separating patients with true structural heart disease from those with unusual variations who are abnormal only in a statistical sense.

Other findings such as right bundle-branch block (RBBB), are present in patients with heart disease but also occur frequently in patients who have no evidence of heart disease by history, physical examination, or echocardiography.

2 What is the differential diagnosis for low voltage?

Chronic obstructive pulmonary disease, hypothyroidism, pericardial effusion, anasarca, amyloidosis, ischemic cardiomyopathy, and obesity are included in the differential diagnosis.

3 Is electrocardiography sensitive or insensitive for detecting chamber enlargement and hypertrophy?

It is insensitive. When echocardiography or autopsy is used as the gold standard, ECG misses many patients with real chamber enlargement or hypertrophy. This is particularly true with patients who have less severe (yet still potentially meaningful) degrees of these findings. Although useful because of low cost and ease of application, electrocardiography certainly has its limitations.

4 Which clues suggest that a patient may have left ventricular hypertrophy?

High QRS voltage is the hallmark of left ventricular hypertrophy (LVH), although many young patients have high QRS voltage without real LVH. Other associated hints (albeit nonspecific) are left axis deviation, left atrial enlargement, widening of the QRS, and strain (associated ST-T abnormalities).

Patients with left bundle-branch block (LBBB) cannot be diagnosed with LVH from the ECG, but it is important to remember that many patients with LBBB actually have LVH by echocardiography. There are a number of scoring systems to decide whether a patient meets ECG criteria for LVH, and all of them are insensitive.

5 An adult has a large R wave in V1. What is the differential diagnosis?

image Right ventricular hypertrophy (look for associated right axis deviation, right atrial enlargement, and right ventricular (RV) strain with ST-T abnormalities)
image Posterior myocardial infarction
image Wolff-Parkinson-White (WPW) syndrome
image Muscular dystrophy
image Normal early transition

6 What leads are most helpful when looking for a bundle-branch block?

image V1, V6, I, and to some extent II
image The QRS duration should be more than 120 ms to identify a bundle-branch block. Not every wide QRS is a bundle-branch block; the differential diagnosis also includes a ventricular beat, intraventricular conduction delay, hyperkalemia, drug effect, and WPW with conduction through an accessory pathway.

7 What are the characteristics of a right bundle-branch block?

Patients with RBBB typically have an rSR′ pattern in V1 and a broad terminal S wave in I and V6 (Figure 22-1).

image

Figure 22-1 Typical appearance of a right bundle-branch block in V1, with rSR′.

8 What is an intraventricular conduction delay? When is it seen?

An intraventricular conduction delay is a wide QRS that arises from supraventricular conduction that is neither a typical RBBB nor a typical LBBB. It is often noted in patients with a cardiomyopathy.

9 What are the characteristics of a left bundle-branch block?

In V1 there is a broad, deep S wave (or QS wave), with ST segment elevation, that may be preceded by a very narrow R wave (Figure 22-2). In lead I there is a broad R wave (sometimes notched) without a Q or S wave.

image

Figure 22-2 Typical appearance of a left bundle-branch block in V1. In some cases a narrow R wave precedes the large monomorphic S wave.

10 What is a hemiblock?

The left bundle bifurcates into two fascicles (anterior and posterior), and either one may be blocked. With a hemiblock the QRS duration is generally less than 120 milliseconds unless there is an associated RBBB (commonly termed a bifascicular block).

11 You are attempting to pass a Swan-Ganz catheter into the pulmonary artery in a patient with LBBB. When the hemodynamic tracing suggests that the catheter tip is in the right ventricle, the patient suddenly becomes bradycardic, with a heart rate of 25. What happened?

The patient is probably in complete heart block as a result of a catheter-induced RBBB (together with a preexisting LBBB). Fortunately the injury to the right bundle branch is often brief, but temporary pacing may be required.

For patients with LBBB, consider the value of a pulmonary artery catheter carefully before proceeding. In addition, you should have emergency pacing equipment readily available to respond properly if this complication develops. Transient stunning of the right bundle may occur in as many as 5% to 10% of cases.

12 Does a normal ECG exclude the possibility of severe coronary artery disease?

No, although an ECG done during ischemic chest pain is usually abnormal. It is common for patients with severe coronary artery disease (CAD) to have an ECG with only nonspecific abnormalities.

For an example of ECG findings noted in a patient with exertional angina, see Figure 22-3.

image

Figure 22-3 This 12-lead ECG shows deep relatively symmetric T wave inversions, meeting ECG criteria for ischemia. Coronary insufficiency is generally the most common life-threatening cause of this pattern. Not uncommonly patients with chest pain at rest from coronary insufficiency (an acute coronary syndrome) may present with an ECG like this. They might also present with ST segment depression, nonspecific ST-T abnormalities, or even a normal ECG. Although deep symmetric T inversions should generally provoke a clinical evaluation for coronary disease, other causes should be considered, including pulmonary embolus, acute central nervous system pathology (classically a subarachnoid bleed), a cardiomyopathy, abnormal repolarization from ventricular hypertrophy, or significant electrolyte disturbances. This patient was a 42-year-old woman with history of smoking who presented with progressive angina, occurring with only minimal exertion. Catheterization showed severe multivessel disease for which she underwent coronary artery bypass surgery.

13 How are patients with myocardial infarction subdivided on the basis of ECG changes during infarction?

Myocardial infarctions (MIs) are often divided into two types: ST segment elevation MI and non-ST segment elevation MI. Patients with ST segment elevation should be considered for immediate percutaneous coronary intervention (PCI), or thrombolytic therapy if PCI is unavailable. Q waves usually develop over time in the leads where there is elevation. Q waves may diminish in size or go away over time. Patients with acute MI without ST elevation often have ST-segment depression (which may be dynamic) and/or T-wave inversions. Patients with non-ST-elevation MI can usually be made pain-free with medical therapy, and cardiac catheterization is often performed within several days. However, ongoing symptoms and ECG changes refractory to medical therapy can prompt emergent invasive evaluation.

For an example of ECG changes associated with a non-ST segment elevation MI, see Figures 22-4 and 22-5.

Buy Membership for Anesthesiology Category to continue reading. Learn more here

Related posts:

58: Congenital Heart Disease 59: Fundamentals of Obstetric Anesthesia 34: Heart Failure 5: Electrolytes 76: Electroconvulsive Therapy 41: Acute Respiratory Distress Syndrome (ARDS)