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![<bold>Figure 2.</bold>](/view/journals/anpr/63/2/inline-i0003-3006-63-2-95-f02.png)
Medtronic MRI-compitable pacemaker.
![Figure.](/view/journals/anpr/70/2/inline-i1878-7177-70-2-70-f01.png)
A 12-lead electrocardiogram (ECG) obtained soon after the patient's condition initially deteriorated.
Idioventricular pattern noted on the ECG along with pacing failure. Heart rate was approximately 30 beats/min. Regularly spaced red arrows indicate pacemaker spikes that were occurring despite lack of capture.
![Figure 17.](/view/journals/anpr/53/2/inline-i0003-3006-53-2-53-f17.gif)
Third-degree (complete) block. There are P waves but the PR intervals appear inconsistent; no pattern is repeated. If impulses were being conducted into the ventricles, the R-R intervals would be irregular and the QRS complexes would be narrow. Neither is the case, however; the R-R intervals are regular and the complexes are slightly widened. (They get wider and wider according to the location of the ventricular pacemaker. In this case, the pacer is probably in the bundle of His, because the complex is relatively narrow.) On closer analysis, one can detect that intervals between P waves (P-P intervals) are consistent and that R-R intervals are consistent. The only explanation is that the SA node is pacing the atria but impulses are not reaching the ventricles. Therefore, the ventricles have developed their own pacemaker and we have a complete (third-degree) heart block.
![Figure 8.](/view/journals/anpr/53/2/inline-i0003-3006-53-2-53-f08.gif)
Junctional rhythm. There are no P waves and a PR interval cannot be ascertained. Therefore, the sinoatrial node is not pacing this rhythm. But the QRS complexes are narrow, so the pacemaker is above the ventricles. The logical conclusion is that the atrioventricular node or neighboring tissue is pacing the heart. This is called junctional rhythm. Because this node has a slower firing rate than the sinoatrial node (See Figure 1), rates of 50 and 90 are the cutoffs for bradycardic and tachycardic rates, ie, junctional bradycardia or tachycardia.
![Figure 11.](/view/journals/anpr/53/2/inline-i0003-3006-53-2-53-f11.gif)
Atrial flutter. Multiple waves appear between each QRS complex and we cannot ascertain whether they are P or T waves. This pattern emerges when an ectopic pacemaker emerges in the atrial muscle and fires more rapidly than the sinuatrial node. This generates multiple depolarizations in the atrial muscle, reflected as so-called flutter waves. Each has a slant to its anterior portion; we can describe this as a saw-toothed pattern. Normally, the atrioventricular node allows only one of them to pass into the ventricle each cycle, which results in a regular ventricular response.
![Figure 13.](/view/journals/anpr/53/2/inline-i0003-3006-53-2-53-f13.gif)
Atrial fibrillation. The waves between each QRS complex are random and indistinct; in essence, they're a mess! Furthermore, the R-R intervals are consistently irregular. This pattern emerges when several ectopic pacemakers emerge in the atrial muscle and all fire more rapidly than the sinuatrial node. This generates multiple depolarizations in the atrial muscle, far more numerous than those with atrial flutter. The atrioventricular node is so overwhelmed with impulses that it cannot allow any to pass through on a regular basis. Therefore, we see this striking irregular ventricular response.
![Figure 7.](/view/journals/anpr/59/2/inline-i0003-3006-59-2-90-f07.png)
Cardiovascular effects of epinephrine.31 The following graph illustrates the typical cardiovascular response to epinephrine administered as a continuous intravenous infusion of 10 µg/min. (This is the amount contained in 1 mL of a 1 ∶ 100,000 concentration.) Epinephrine increases heart rate (HR) by activating beta-1 receptors in the sinoatrial node, the heart's normal pacemaker. It also activates beta-1 receptors on myocardial cells, increasing their contractility and increasing systolic blood pressure (SBP). However, it activates beta-2 receptors on systemic arteries producing vasodilation. This decline in arterial resistance produces a reduction in diastolic pressure (DBP). These effects result in little change of mean arterial pressure (MAP).
![Figure 12.](/view/journals/anpr/53/2/inline-i0003-3006-53-2-53-f12.gif)
Premature atrial and junctional complexes. Most cycles commence with a P wave, and most PR intervals are normal. Therefore, the rhythm is sinus-paced, but occasionally an extra impulse is fired from an ectopic pacemaker that travels down into the ventricle and creates an extra QRS complex. Notice that normally there is a pause, or a period of time following a T wave until the next P wave commences. In the case of premature complexes, this pause is interrupted. At this point in your training, it is not important to interpret the source of this premature complex; is it atrial or junctional? We know it is coming from above the ventricle, and it is always acceptable to call it a premature atrial complex. The difference between the two has little clinical relevance.
![Figure 18.](/view/journals/anpr/53/2/inline-i0003-3006-53-2-53-f18.gif)
Premature ventricular complexes. Most cycles contain narrow QRS complexes and could represent any of the supraventricular rhythms described in groups A or B. But occasionally one sees a wide QRS complex interposed between the cardiac cycles. Therefore, the primary rhythm may be sinus- or supraventricular-paced, but occasionally an extra impulse is fired from an ectopic pacemaker within the ventricle and creates a wide QRS complex. These complexes are called premature ventricular complexes and may accompany any of the supraventricular rhythms described thus far. If the complexes on a tracing all resemble one another in shape, a single irritable focus is the culprit and is described as unifocal. If the premature ventricular complexes have variable shapes, multiple foci are implicated and the rhythm is described as multifocal.