Sinus P wave

If you find a P wave in the pause, check to see whether it s premature or it occurs earlier than subsequent sinus P waves. If it s premature (see the shaded area in the top rhythm strip), you can be sure it s a nonconducted PAC. 

The PAC occurs earlier than the sinus P wave, with an abnormal configuration when compared with a sinus P wave (see shaded area below). 

Figure 12.4 Base-apex electrocardiograms from an anaesthetized horse, with endotoxemia caused by a strangulating intestinal lesion, (a) The cardiac rhythm was converted from ventricular tachycardia to the bigeminal rhythm by administration of two bolus doses of lidocaine. Although ventricular complexes (V) are preceeded by p waves (p) the p-r distance is shorter than the sinus complexes (S). (b) Magnesium sulfate administered intravenously resulted in conversion to sinus rhythm.

Figure 4.54 (A) Preoperative ECG of a 58-year-old patient without heart disease. (B) In a postoperative period the patient suffered from massive pulmonary embolism with the ECG showing an AQRS pointing sharply to the right, complete right bundle branch block with the ST-segment elevation in some leads and sinus tachycardia. The P wave is visible in the majority of leads with occasional premature beats. (C) Patient died within minutes the ECG in agonic rhythm.

Sinus node reentry or intraatrial reentry occur less commonly, and neither is as well described as AV nodal or AV reentry. Aside from a characteristic abrupt onset and termination, coupled with subtle changes in P-wave morphology, these tachycardias can be difficult to diagnose. Electrophysiologic studies may be necessary to determine the ultimate mechanism of the PSVT. 

Automatic atrial tachycardias such as multifocal atrial tachycardia appear to arise from supraventricular foci that have enhanced automatic properties. It is presumed that multifocal atrial tachycardia is the result of multiple ectopic atrial pacemakers, which account for the variable and differing P-wave morphology. In unifocal atrial tachycardia (sometimes referred to as ectopic atrial tachycardia), a single P-wave morphology different from that of sinus rhythm is recorded. In either case, the underlying, precipitating disorder present in the major-... 

Fig. 3.4 VDD mode. Sensing occurs in both the atrium and the ventricle but pacing only occurs in the ventricle. Atrial events may be tracked and followed by ventricular-paced events (PV). When there is a sinus pause or a PVC not followed by a P wave, the next event will be a ventricular-paced event rather than an atrial-paced event in DDD mode. The AV and PV intervals can be programmed separately in some pulse generators.

Fig. 10.4 Representative Holter recordings from an asymptomatic patient with a type I block variant that was misdiagnosed as type II block by several physicians. (A) Type I block with constant PR intervals before the blocked beat. Note that there is a slight increase in the sinus rate in the seqnence before the blocked beat. However, the sinus rate then slows down and the blocked P-wave occurs in association with sinus slowing a combination consistent with a vagal phenomenon. The PR intervals after the blocked beat are inconstant. (B) Type I variant simulating type II block. The PR intervals are constant before and after the blocked beat. However, there is obvious sinus slowing simultaneously with the nonconducted P-wave. (C) Type I block. Note that in the presence of a narrow QRS complex, the occurrence of type I (with fairly large increments of the PR intervals) and what appears to be type II block basically rules out the presence of a true type II block.

Fig. 10.5 Sinus rhythm with second-degree Type 13 2 iniranodal AV block, and RBBB. Note that the AH interval remains constant. TTie HV interval increases from 80 (following first P-wave) to 150ms (following second P-wave). The third P-wave is followed by an H deflection but no QRS complex. AV block occurs in the His-Purkinje system below the site of recording of the His bundle potential (arrow). Note the shorter PR interval after the nonconducted P-wave, a feature typical of Type I second-degree AV block. HBE = His bundle electrogram, A = atrial deflection, H = His bundle deflection, V = ventricular deflection, P = P-wave. TL = time lines 50ms. (Barold SS. Pacemaker treatment of bradycardias and selection of optimal pacing modes. In Zipes DP (Ed.). Contemporary Treatments in Cardiovascular Disease, 1997 1 123, with pamission.)...

Fig. 10.8 Narrow QRS type I block registered in a 3-lead Holier recording. There is sinus arrhythmia. The last three PR intervals before the blocked beat (arrow) are constant. This pattern should not be classified as type II block when conduction of the postblock P-wave is not seen. Actually the P-wave after the block was conducted with a shorter PR interval consistent with type I block.

The differential diagnosis of this regular narrow QRS complex rhythm with 1 1 AV relationship at such a short interval between R and P waves is essentially typical AV node reentrant tachycardia (AVNRT) vs. atrial tachycardia with a severe first degree AV block. The interval between each R wave and subsequent P wave appears fixed. An atrial or sinus tachycardia does not have this fixed relationship between R and subsequent P wave, and typically may display variation in the interval between them. Thus, from the EGMs this is most likely typical AVNRT. 

A tachycardia with R wave morphology identical to that in sinus rhythm and near-simultaneous activation of the ventricles, then the atria with each beat is seen. This is most likely typical AVNRT, however initiated after two PVCs that conduct retrogradely to the atria. The retrograde P waves act like PACs and initiate the rhythm. 

Most bedside monitoring systems allow for simultaneous monitoring of two leads, such as lead II with or MCL. Lead II or the lead that clearly shows the P waves and QRS complex may be used for sinus node arrhythmias, PACs, and AV block. The precordial leads V. and Vg or the bipolar leads MCL. and MCLg are the best leads for monitoring rhythms with wide QRS complexes and for differentiating VT from SVT with aberrancy. 

A 72-year-old woman, treated with flecainide and haloperidol, presented with breathlessness due to regular tachycardia with wide QRS complex. The ECG showed a regular monomorphic tachycardia at ISObpm, no apparent P wave, QRS duration of 240 ms with a left bxmdle branch block. An intravenous bolus of 10 mg ATP was administered. However, it turned out to be ineffective. The diagnosis of tachycardia induced by flecainide overdose was considered and treatment with 8.4% sodium bicarbonate was initiated. The sodium bicarbonate infusion caused immediate narrowing of the patienPs QRS and the ECG showed sinus rhythm. Blood samples confirmed flecainide overdose [27]. 

Originate from the His bundle or the AV junction. The impulse may activate the ventricles via the normal pathway. Alternatively the atria may also be activated by retrograde conduction. This is where the impulse travels back up towards the atria instead of down towards the ventricles activating the atria. Junctional pranature beats can be seen on the ECG as they occur before the next normal sinus beat. Often there is no P wave present if the atria and ventricles are depolarised simultaneously, as this is masked by the QRS complex (Fig. 6.3). Alternatively the P wave may be inverted (Fig. 6.4) and can occur either before, or after the QRS complex (Fig. 6.5). 

Caused by the inability of the SAN to activate the atiia, leading to an absence of P waves on the ECG. These blocks can be classified as either complete or incomplete SA blocks. Incomplete blocks cause the occasional loss of beats. Complete SA block occurs when no impulses leave the SAN leading to Sinus Arrest , a complete lack of heart beats (no PQRS or T waves present). 

The intermittent absence of atrial activation causes a gap or pause on the ECG. This pause is either caused by a gradual reduction in the P to P interval (the distance between one P wave and the next). This results in a pause, the cycle then continues. This is also known as type I sinus exit block (Fig. 7.13). 

The other form of incomplete SA block, known as type II sinus exit block is determined due to its mathematical relationship with the conduction cycle. In this type of SA block there is no shortening of the P to P interval but instead an unexpected absence of a P wave and subsequent QRS complex. The pause is multiple of the P to P interval (Fig. 7.14). 

Serum protein electrophoresis — increased or2 globulin serum aspartate aminotransferase 90 IU/1. The fasting plasma was turbid, triglycerides 3.8 mmol/1, lipoprotein electrophoresis — increased pre- band ECG. — sinus tachycardia 120/min and peaked P waves. The clinical diagnosis of Refsum s disease was confirmed by the finding of large amounts of phytanic acid in the patient s plasma (vide infra). 

Useful for P wave identification detecting sinus node arrhythmia, atrial arrhythmia, and monitoring the inferior wall of the left ventricle. 

Lead II or the best lead that clearly shows P waves and the QRS complex may be used for sinus node arrhythmias, premature atrial contractions, and atrioventricular block... 

WARNING Long-acting p2-agonists may t risk of asthma-related death Uses COPD maint Action LA p2-agonist, relaxes airway smooth muscles Dose 15 meg neb bid, 30 meg/d max Caution [C, ] w/ CV Dz, X Contra Not for acute asthma component hyp sensitivity peds w/ phenothiazines Disp Meg neb SE Chest/back pain, D, sinusitis, leg cramps, dyspnea, rash, flu-synd, t BP, arrhythmias, heart block J-K EMS Monitor ECG for arrhythmias, heart block, and hypokalemia (flattened T waves) t risk of acute asthma attack, treat w/ shortacting p-agonist OD May cause CP, palpitations, muscle tremors and cramps, and syncope symptomatic and supportive... 

As we have discussed previously ( cardiac memory in the intermittent LBBB and WPW syndrome), patients with intermittent right-ventricular stimulation, when the stimulus is conducted via the normal path (Figure 3.35), can show a cardiac memory phenomenon (lack of adequacy of the repolarisation to the depolarisation changes), which explains the anomalous repolarisation (negative T wave) that is sometimes observed, in sinus rhythm in the absence of IHD. It has been demonstrated that in this situation, the T wave is negative in precordial lead but is positive in I and VL (see Figure 3.35, p. 52). 

Similar ECG patterns with transient ST-segment elevation and q wave may be seen in myocarditis (Figure 5.47). However, the QTc interval in myocarditis is usually normal, the voltage of QRS is also usually very low and there is usually sinus tachycardia. Furthermore, in myocarditis the angiographic features are not present. Also, recently, some cases of acute ST-segment elevation have been described in patients with catecholamine discharge and stroke, sometimes with chest pain. In these cases, a transient dyskinesia of basal part of the heart has been found (p. 274). 

---