**3. Arrhythmic complications of PICC line**

The innate properties of neonatal myocardium predispose to different types of arrhythmia. Cardiac arrhythmias are rare but potentially life-threatening. Hence, should be identified and intervened immediately by the bedside neonatologist, especially when it occurs with an indwelling central venous catheter. Even though many neonatal literature mentions about the risk of arrhythmias with centrally placed catheters in neonates, the incidence is less known. Until now 16 cases of central venous catheter-induced arrhythmias are reported, with tachyarrhythmias being the commonest form. The most common arrhythmias reported so far are atrial flutter (8/16) and supraventricular tachycardia (7/16) [6, 7].

#### **3.1. The timing of arrhythmias with the central line**

Arrhythmias may occur anytime, from the time of insertion of central catheters till the time of withdrawal (**Table 1**).


**3.** Anytime at the indwelling phase due to migration/dislodgement of central venous catheters.

Cases were documented from within few minutes after insertion till 47 days post insertion of central venous catheter (CVC) [16, 17].

#### **3.2. Proposed mechanism of arrhythmia induction**

Typically the etiology lies on inappropriately placed intracardiac catheters in all the cases.

The possible mechanisms are


#### **3.3. Types of cardiac arrhythmias induced by intracardiac central venous catheter**

Malpositioned, migrated or inappropriately placed central venous catheter can cause a wide range of arrhythmias ranging from tachyarrhythmias to bradyarrhythmias as mentioned in **Figure 4**.

#### *3.3.1. Tachyarrhythmia*

cardiac shadow immediately after taking X-ray. After adjustment of the catheter tip, confirmatory X-ray is mandatory. Massive pleural effusion and pericardial effusion has been reported

**Figure 3.** PICC line with intracardiac looping. Chest X-ray shows left PICC line passed superior vena cava, got looped

The innate properties of neonatal myocardium predispose to different types of arrhythmia. Cardiac arrhythmias are rare but potentially life-threatening. Hence, should be identified and intervened immediately by the bedside neonatologist, especially when it occurs with an indwelling central venous catheter. Even though many neonatal literature mentions about the risk of arrhythmias with centrally placed catheters in neonates, the incidence is less known. Until now 16 cases of central venous catheter-induced arrhythmias are reported, with tachyarrhythmias being the commonest form. The most common arrhythmias reported so far

Arrhythmias may occur anytime, from the time of insertion of central catheters till the time

**1.** Procedural phase: due to advancement beyond SVC. It commonly happens due to improper measurement. Willful over advancement of the catheter into the intracardiac chamber with the hope to withdraw the catheter after radiographic confirmation is one of the com-

**2.** Securing phase—migration to the intracardiac chamber can occur due to handling during

following an inappropriately placed PICC lines [1, 14].

**3. Arrhythmic complications of PICC line**

**3.1. The timing of arrhythmias with the central line**

mon practices which should be forbidden.

of withdrawal (**Table 1**).

in right atrium.

164 Cardiac Arrhythmias

the time of fixation.

are atrial flutter (8/16) and supraventricular tachycardia (7/16) [6, 7].

Tachyarrhythmias are abnormal fast rhythms originating from atria or from ventricles of the heart. With intracardiac indwelling catheters, tachyarrhythmias are more common than bradyarrhythmias. Recognition of tachyarrhythmia is crucial for any intensivist. If not identified in time, it may end up with congestive cardiac failure due to significantly compromised cardiac output due to incessant tachycardia. Cardiogenic shock may happen due to


**Table 1.** Timing of development of arrhythmias with central line.

**Figure 4.** Types of Cardiac arrhythmias induced by centra lines.


**Table 2.** Normal heart rate variations in neonates.

prolonged myocardial hypoxia. It manifests as effortless tachypnoea, tachycardia (earliest sign), poor perfusion, prolonged capillary refill time, bilateral crepitations and hypotension (late sign).

Knowledge of normal heart rate is essential before diagnosing any tachyarrhythmia. Normal heart rate varies in newborn widely (**Table 2**).

**Normal sinus rhythm**: normal heart rate for a newborn varies from 120 to 205 in an awake state. Normal sinus rhythm is characterized by upright P wave in lead I and a VF which is followed by narrow QRS complexes.

#### **3.4. Classification of tachyarrhythmia**

Tachyarrhythmia is classified into supraventricular tachycardia/atrial tachyarrhythmia, junctional tachycardia and ventricular tachycardia depending on where the arrhythmic impulses emanate from (**Figure 5**). Any of the mentioned tachyarrhythmia depicted in **Figure 5** can occur due to above-mentioned mechanisms.

For clinical purpose, tachyarrhythmias are classified based on QRS complex in the ECG (**Table 3**).

ventricular tachycardia. The management is different for each type of tachyarrhythmia. Important arrhythmias induced by central lines are described here, explaining other rare

**1.**Ventricular tachycardia

**2.**Supraventricular tachycardia with aberrant conduction

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forms are out of the scope of this chapter.

**Table 3.** Clinical classification of tachyarrhythmias.

**Narrow QRS complex (≤80 ms) Wide QRS complex (>80 ms)**

**Figure 5.** Types of Tachyarrhytmias.

**3.**Supraventricular tachycardia

**1.**Sinus tachycardia **2.**Atrial flutter

The essential part of treating any tachyarrhythmia is based on differentiating different types of tachyarrhythmia like sinus tachycardia, supraventricular tachycardia, atrial flutter and

**Figure 5.** Types of Tachyarrhytmias.

prolonged myocardial hypoxia. It manifests as effortless tachypnoea, tachycardia (earliest sign), poor perfusion, prolonged capillary refill time, bilateral crepitations and hypotension

**Age Awake rate (bpm) Mean Sleeping rate** Newborn to 3 months 85–205 140 80–160

Knowledge of normal heart rate is essential before diagnosing any tachyarrhythmia. Normal

**Normal sinus rhythm**: normal heart rate for a newborn varies from 120 to 205 in an awake state. Normal sinus rhythm is characterized by upright P wave in lead I and a VF which is

Tachyarrhythmia is classified into supraventricular tachycardia/atrial tachyarrhythmia, junctional tachycardia and ventricular tachycardia depending on where the arrhythmic impulses emanate from (**Figure 5**). Any of the mentioned tachyarrhythmia depicted in **Figure 5** can

For clinical purpose, tachyarrhythmias are classified based on QRS complex in the ECG

The essential part of treating any tachyarrhythmia is based on differentiating different types of tachyarrhythmia like sinus tachycardia, supraventricular tachycardia, atrial flutter and

(late sign).

166 Cardiac Arrhythmias

(**Table 3**).

heart rate varies in newborn widely (**Table 2**).

**Figure 4.** Types of Cardiac arrhythmias induced by centra lines.

followed by narrow QRS complexes.

**Table 2.** Normal heart rate variations in neonates.

**3.4. Classification of tachyarrhythmia**

occur due to above-mentioned mechanisms.


**Table 3.** Clinical classification of tachyarrhythmias.

ventricular tachycardia. The management is different for each type of tachyarrhythmia. Important arrhythmias induced by central lines are described here, explaining other rare forms are out of the scope of this chapter.

#### *3.4.1. Sinus tachycardia*

Sinus tachycardia can arise at the rate of 180–220 bpm. It arises due to stimulation of SA node typically due to body's response to the need of increased cardiac output. It can arise in response to any stress, pain, hyperthermia, anemia, commonly used drugs like caffeine and more. It must be differentiated from other pathological causes by means of Normal P waves, variable R-R interval, constant PR interval, precipitating factors like fever, sepsis, and failure to respond with vagal maneuvers.

secondary to the malposition of the catheter, the first step of management should be to pull back or even remove the catheter. If the neonate is hemodynamically unstable, the best treatment option will be synchronized cardioversion with a dose of 0.5 J/kg. If the neonate is hemodynamically stable, digoxin therapy can be used as a first line management. The response rate for digoxin is roughly around 33%. Many times atrial flutter needs permanent reversion to DC cardioversion. Intravenous adenosine can be used to terminate the arrhythmia which uncovers a flutter in SVT. Occasionally esophageal overdrive pacing may

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Narrow complex SVT is the most common type of hemodynamically significant arrhythmia in neonates. With better modes of detection and high index of suspicion, the incidence of SVT is now estimated to be 1 in 200–250 neonates. In SVT the impulses are originating proximal to the bundle of His. The typical infant who has SVT has a regular R-R interval, with rates often greater than 230 beats/min and commonly 260–300 beats/min. The atrial and ventricular rates are equal. They are further sub-classified by the inducing mechanisms into either automatic or re-entry. Most SVTs are re-entry type atrioventricular SVTs utilizing an accessory pathway. Commonly the impulses travel down the AV node and retrogradely up the accessory path-

Management depends on the hemodynamic status of the neonate. As the arrhythmia occurred secondary to the malposition of the catheter, the first step of management should be to pull back or even remove the catheter. If the neonate is relatively stable, the next step is to stop the re-entry loop (as most of the neonates with SVT have atrioventricular re-entry tachycardia) by inducing vagal maneuvers. One can perform vagal maneuvers like keeping crushed ice inside two plastic bags and place the ice pack over the face carefully for few minutes. Oropharyngeal suction can be used to stimulate the vagus. The use of vagal maneuvers in neonates are controversial, but still one can use for buying time of adenosine preparation. Pressure on eyeballs and carotid sinus massage should not be attempted in neonates, as this may cause retinal detachment and cerebral ischemia [6, 15, 16]. If tachycardia persists, the initial step of management is stabilizing the neonate (intubation/assisted ventilation/check the blood pressure and do ABG) followed by administration of intravenous adenosine. Adenosine can be given in a starting dose of 0.05 mg/kg and can be increased by 0.05 mg/kg up to 0.25 mg/kg. The dosage can be increased up to 0.3 mg/kg for recalcitrant cases with a cardiologist approval. Recent literature suggests the starting dose of adenosine as 0.1 mg/kg

**Figure 7.** Supra ventricular tachycardia. Lead II ECG: absent P wave, narrow QRS complex and constant R-R interval.

be required [7, 8, 17].

way (**Figure 7**) [15, 16].

*3.4.2.2. Supraventricular tachycardia (SVT)*

with the maximum of 0.5 mg/kg [8, 9].

#### *3.4.2. Atrial tachycardia*

Atrial tachycardia arises when the impulses emanate from the atrium, specifically the right atrium. Atrial excitations have a very low threshold potential in preterm infants. Thereby whenever irritated by any mechanical stimuli, for example, a central venous catheter, atrial tachyarrhythmia occurs more often. The true two forms of atrial tachycardia are atrial flutter and atrial ectopy.

#### *3.4.2.1. Atrial flutter*

Atrial flutter is the common rhythm induced by the intracardiac position of PICC line and an awareness of this pattern is crucial for a neonatologist. Atrial flutter is best described by regular rapid atrial rates of 240–360 beats/min. The electrocardiogram (ECG) will show a regular rhythm with a sawtooth pattern of P waves otherwise known as the typical flutter waves. It is best seen in lead II, lead III and aVF leads with a long strip ECG. The QRS complex will be narrow if there is no aberrant pathway (**Figure 6**).

In neonates, atrial flutter commonly causes 2:1 AV conduction block. It may also cause various degrees of AV block. Atrial flutter in a non-catheter related context is less common than SVT. So it is potentially prone to under-recognition. A 12-h time of incessant tachycardia is enough to decompensate the hemodynamic status of a neonate. The chances of developing cardiac failure depend on the duration of arrhythmia, structural nature of the heart and gestational age rather than the rate alone. One has to quickly recognize atrial flutter and able to differentiate from SVT as the treatment option varies for both, with synchronized cardioversion for atrial flutter and adenosine for SVT [7, 8, 17].

Management depends on proper identification of atrial flutter, assessing the hemodynamic status of the neonate and recognition of treatable causes. As the arrhythmia occurred

**Figure 6.** Atrial flutter. Lead II ECG: sawtooth flutter waves.

secondary to the malposition of the catheter, the first step of management should be to pull back or even remove the catheter. If the neonate is hemodynamically unstable, the best treatment option will be synchronized cardioversion with a dose of 0.5 J/kg. If the neonate is hemodynamically stable, digoxin therapy can be used as a first line management. The response rate for digoxin is roughly around 33%. Many times atrial flutter needs permanent reversion to DC cardioversion. Intravenous adenosine can be used to terminate the arrhythmia which uncovers a flutter in SVT. Occasionally esophageal overdrive pacing may be required [7, 8, 17].

#### *3.4.2.2. Supraventricular tachycardia (SVT)*

*3.4.1. Sinus tachycardia*

168 Cardiac Arrhythmias

*3.4.2. Atrial tachycardia*

and atrial ectopy.

*3.4.2.1. Atrial flutter*

to respond with vagal maneuvers.

narrow if there is no aberrant pathway (**Figure 6**).

sion for atrial flutter and adenosine for SVT [7, 8, 17].

**Figure 6.** Atrial flutter. Lead II ECG: sawtooth flutter waves.

Sinus tachycardia can arise at the rate of 180–220 bpm. It arises due to stimulation of SA node typically due to body's response to the need of increased cardiac output. It can arise in response to any stress, pain, hyperthermia, anemia, commonly used drugs like caffeine and more. It must be differentiated from other pathological causes by means of Normal P waves, variable R-R interval, constant PR interval, precipitating factors like fever, sepsis, and failure

Atrial tachycardia arises when the impulses emanate from the atrium, specifically the right atrium. Atrial excitations have a very low threshold potential in preterm infants. Thereby whenever irritated by any mechanical stimuli, for example, a central venous catheter, atrial tachyarrhythmia occurs more often. The true two forms of atrial tachycardia are atrial flutter

Atrial flutter is the common rhythm induced by the intracardiac position of PICC line and an awareness of this pattern is crucial for a neonatologist. Atrial flutter is best described by regular rapid atrial rates of 240–360 beats/min. The electrocardiogram (ECG) will show a regular rhythm with a sawtooth pattern of P waves otherwise known as the typical flutter waves. It is best seen in lead II, lead III and aVF leads with a long strip ECG. The QRS complex will be

In neonates, atrial flutter commonly causes 2:1 AV conduction block. It may also cause various degrees of AV block. Atrial flutter in a non-catheter related context is less common than SVT. So it is potentially prone to under-recognition. A 12-h time of incessant tachycardia is enough to decompensate the hemodynamic status of a neonate. The chances of developing cardiac failure depend on the duration of arrhythmia, structural nature of the heart and gestational age rather than the rate alone. One has to quickly recognize atrial flutter and able to differentiate from SVT as the treatment option varies for both, with synchronized cardiover-

Management depends on proper identification of atrial flutter, assessing the hemodynamic status of the neonate and recognition of treatable causes. As the arrhythmia occurred Narrow complex SVT is the most common type of hemodynamically significant arrhythmia in neonates. With better modes of detection and high index of suspicion, the incidence of SVT is now estimated to be 1 in 200–250 neonates. In SVT the impulses are originating proximal to the bundle of His. The typical infant who has SVT has a regular R-R interval, with rates often greater than 230 beats/min and commonly 260–300 beats/min. The atrial and ventricular rates are equal. They are further sub-classified by the inducing mechanisms into either automatic or re-entry. Most SVTs are re-entry type atrioventricular SVTs utilizing an accessory pathway. Commonly the impulses travel down the AV node and retrogradely up the accessory pathway (**Figure 7**) [15, 16].

Management depends on the hemodynamic status of the neonate. As the arrhythmia occurred secondary to the malposition of the catheter, the first step of management should be to pull back or even remove the catheter. If the neonate is relatively stable, the next step is to stop the re-entry loop (as most of the neonates with SVT have atrioventricular re-entry tachycardia) by inducing vagal maneuvers. One can perform vagal maneuvers like keeping crushed ice inside two plastic bags and place the ice pack over the face carefully for few minutes. Oropharyngeal suction can be used to stimulate the vagus. The use of vagal maneuvers in neonates are controversial, but still one can use for buying time of adenosine preparation. Pressure on eyeballs and carotid sinus massage should not be attempted in neonates, as this may cause retinal detachment and cerebral ischemia [6, 15, 16]. If tachycardia persists, the initial step of management is stabilizing the neonate (intubation/assisted ventilation/check the blood pressure and do ABG) followed by administration of intravenous adenosine. Adenosine can be given in a starting dose of 0.05 mg/kg and can be increased by 0.05 mg/kg up to 0.25 mg/kg. The dosage can be increased up to 0.3 mg/kg for recalcitrant cases with a cardiologist approval. Recent literature suggests the starting dose of adenosine as 0.1 mg/kg with the maximum of 0.5 mg/kg [8, 9].

**Figure 7.** Supra ventricular tachycardia. Lead II ECG: absent P wave, narrow QRS complex and constant R-R interval.

#### *3.4.2.3. Relevant facts about adenosine*


#### **3.5. Bradyarrhythmia**

As depicted in **Figure 8**, bradyarrhythmias may occur either due to contact/injury to the sinoatrial node (SA node) or the atrioventricular node (AV node). So far bradyarrhythmias as complications of central venous catheters are not reported but can happen.

Bradyarrhythmias can be benign but however, acutely unstable bradycardia can lead to cardiac arrest. Management includes identification and correction of reversible causes, pharma-

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AV nodal conduction disturbances can occur due to endocardial irritation by the catheters. It

1. Measure the length of intravascular placement of a catheter for each neonate and document it properly in the case record. If possible, double check it with another physician. **2.** Traditional measurements for PICC line insertion length are based on straight line measurements with bony points using inch tape. These measurements are commonly overestimated,

can lead to bradycardia ranging from first degree to third degree AV block.

**4. Practical tips to minimize the arrhythmic complications**

cotherapy, and rarely cardiac pacing.

**Figure 8.** Types of Bradyarrhythmias.

*3.5.2. AV node*

#### *3.5.1. SA node*

Bradyarrhythmia can occur as a result of SA node dysfunction due to direct injury by the catheter and it can cause complications ranging from first-degree block to sinus arrest.


**Table 4.** Commonly encountered tachyarrhythmia in fetal/neonatal period.

**Figure 8.** Types of Bradyarrhythmias.

Bradyarrhythmias can be benign but however, acutely unstable bradycardia can lead to cardiac arrest. Management includes identification and correction of reversible causes, pharmacotherapy, and rarely cardiac pacing.

#### *3.5.2. AV node*

*3.4.2.3. Relevant facts about adenosine*

170 Cardiac Arrhythmias

continuous ECG monitoring.

concealed pre-excitation.

re-entry mechanism.

**3.5. Bradyarrhythmia**

*3.5.1. SA node*

1. Adenosine is an endogenously available purine nucleoside.

be followed by rapid normal saline flush (5 ml or more).

metabolized rapidly by adenosine deaminase.

**2.** It is a rapidly acting (onset within 20 s) drug with a short half-life of less than 10 s as it is

**3.** It slows the conduction through atrioventricular node and thereby interrupts AV re-entry

**4.** Before giving adenosine place the neonate in mild reverse Trendelenburg position with

**5.** Adenosine must be given as a rapid injection (within 3 s) by peripheral intravenous route directly to the vein. Select the vein which is more proximal to the patient. Injection should

**6.** After conversion of sinus rhythm by adenosine, always save and check the ECG strip for

**7.** If the correct technique is followed, adenosine will terminate 85–93% of SVTs caused by a

**8.** Adenosine is a safe and effective drug with minimal transient side effects. The side effects include flushing (18%), changes in respiration, rarely short bradycardia, hypotension, and

**9.** Adenosine will not terminate the atrial tachycardia. However, it produces transient AV

As depicted in **Figure 8**, bradyarrhythmias may occur either due to contact/injury to the sinoatrial node (SA node) or the atrioventricular node (AV node). So far bradyarrhythmias as

Bradyarrhythmia can occur as a result of SA node dysfunction due to direct injury by the catheter and it can cause complications ranging from first-degree block to sinus arrest.

sweating may occur. Very rarely, short complete AV block can occur.

complications of central venous catheters are not reported but can happen.

**Fetal period SVT and atrial flutter**

Neonatal period (pathological cause) Narrow complex SVT

Indwelling catheter in situ Atrial flutter

**Table 4.** Commonly encountered tachyarrhythmia in fetal/neonatal period.

Neonatal period (generally, they are benign) Premature atrial complexes (PAC)

block which may help to detect atrial flutter (**Table 4**) [8, 9].

pathways and restores normal sinus rhythm within 20 s of its administration.

AV nodal conduction disturbances can occur due to endocardial irritation by the catheters. It can lead to bradycardia ranging from first degree to third degree AV block.
