Viva 8

You have determined a patient requires urgent cardiac pacing. What are the indications for temporary cardiac pacing?

Indications for pacing

  • Asystole or recurrent long sinus pauses
  • Prolonged atrioventricular delay
  • Prolonged QT interval (to prevent torsades de pointes)
  • Hemodynamically unstable bradycardia
  • Bifascicular block(or trifascicular)
  • Mobitz type 2 second degree heart block
  • Recalcitrant VT (for overdrive pacing)
  • Atrial flutter
  • Reentrant SVT
  • Atrial fibrillation or junctional rhythm in diastolic failure
What are the contraindications for transvenous pacing?

These are all relative. Sometimes, one may wish to commence pacing in the face of these contraindications, because the benefits outweigh the risk. Frequently, of course, external pacing is still an option.

  • Excessive risk of bleeding due to vascular access
  • Ongoing bacteraemia (the leads may get infected)
  • Haemodynamically stable bradycardia (i.e. do you really need to pace them?)
  • Large areas of  right ventricular infarction (what tissue will you activate among all that dead myocardium?)
  • Intracardiac thrombus:One might dislodge this either by stimulating the chamber, or by the very act of inserting transvenous pacing lines.
What are the complications of transvenous pacing?
  • Failure to pace, eg. dislodged leads
  • Asynchrony of the chambers (mainly with VVI mode)
  • Vascular access complications, eg. haematoma, pneumothorax etc.
  • Cardiac chamber access problems, eg. knotting in the chamber, or damage to the tricuspid valve
  • Cardiac chamber damage and potential for cardiac tamponade
  • Lead thrombosis and pulmonary embolism
  • Lead infection and infective endocarditis
  • Arrhythmias, eg. VF, VT (due to the leads irritating the tissue)
  • Inadvertent induction of nasty arrhythmia by the pacing itself
  • "Endless loop" reentrant tachycardia
  • Stimulation of the diaphragm and interference with ventilation
Can you explain the difference between unipolar and bipolar pacing?
  • A bipolar circuit has both the electrode inside the heart, with the heart muscle and intraventricular blood completing the circuit.
  • Typically, these electrodes are only about 8mm apart, which reduces the impedance considerably.
  • A unipolar circuit on the other hand has one electrode inside the heart and the other on the surface of the body
  • This relies on a large amount of tissue and body fluid to complete the circuit, and therefore has a much higher impedance.
  • In the majority of situations these days the bipolar circuit is favoured. There is much less electrical interference and substantially less current is required.
Can you describe the technique of inserting a transvenous pacing wire?

The following describes a "blind" technique.

  • You need an introducer sheath, a pulse generator and a pacing catheter.
  • The catheters are mainly bipolar, 3 Fr to 5 Fr in size, and approximately 100 cm in length
  • The catheter is balloon-tipped to assist flotation
  • The balloon holds approximately 1.5 cc of air and should be tested for air leak before insertion.
  • Options of the site of insertion  include the internal jugular, subclavian, femoral, or brachial veins. The right internal jugular and the left subclavian veins are best.
  • First, the introducer is deployed by Seldinger technique.
  • The catheter electrodes are connected directly to the pacing generator.
  • The pacing generator is set with the output to the maximal current, the pacing rate to between 60 and 80 beats/min, and the sensitivity to the lowest level (completely asynchronous).
  • The catheter is advanced through the sheath.
  • If the patient has a pulse, the balloon can be inflated once it has passed through the introducer sheath, approximately at the 20-cm mark (if there is no pulse, it is clearly pointless to inflate the balloon)
  • As the catheter is advanced, the ECG monitor placed on the patient will usually show pacemaker spikes
  • When you hit the RV wall, the ECG should change to an LBBB morphology with every pacing spike followed by an LBBB-ish QRS. We call that "capture".
  • If the balloon was up, it can now be deflated and the catheter secured in place.

There is also a ECG-guided technique (where the tip of the catheter is used as an intracardiac ECG lead to help guide its position) and a fluoroscopic technique.

The characteristic changes in intracardiac ECG morphology are included here for post-viva debrief purposes. The image is from Harrigan et al (2007) with no permission whatsoever.

pacemaker wire placement ecg

After inserting the wire, you notice the pulse generator has been set to AOO mode.
What does this nomenclature mean?
  • Position 1: chamber paced    
  • Position 2: chamber sensed    
  • Position 3: response to sensing

Single chamber pacing modes

  • Single-chamber atrial pacing
    • AOO - asynchronous atrial pacing
    • AAI - atrial demand pacing
    • AAT - atrial pacing
  • Single-chamber ventricular pacing
    • VOO - asynchronous ventricular pacing
    • VVI - ventricular demand pacing
    • VVT - ventricular pacing

Dual chamber pacing modes

  • VAT - atrial sensing, ventricular pacing
  • DDD - dual chamber demand pacing
Nomenclature of Pacing Modes

Position 1: chamber paced

Position 2: chamber sensed

Position 3: response to sensing

O = none

O = none

O = none

A = atrium

A = atrium

T = triggered

V = ventricle

V = ventricle

I = inhibited

D = dual

D = dual

D = dual (triggered and inhibited)

How do you define the term "pacing threshold"?
  • This is the minimum amount of current (in mA) required to initiate depolarization of the paced chamber.
Describe how you would determine the pacing threshold
  • Set the pacemaker well above the native rate, so that the chamber of interest is being paced continuously.
  • Start reducing the output until a QRS complex no longer follows each pacing spike.
  • The output at which there is incomplete capture is the capture threshold.
  • Typically, one might want to set the output to about double capture threshold.
Dow do you define "sensitivity" with regards to the pacemaker?
  • Sensitivity of a pacemaker electrode is the minimum myocardial voltage required to be detected as a P wave or R wave, measured in mV.
  • The lower the number, the more sensitive the pacemaker.
  • The normal settings are 0.4-10mV for the atria, and 0.8-20mV for the ventricles
Describe how you would check the sensitivity of a pacemaker
  • Put the pacemaker in a VVI, AAI or DDD mode (i.e. endogenous cardiac activity should inhibit the pacemaker.)
  • Set the output as low as possible; you don't want to have any R on T phenomena - you only need to see the pacing spikes.
  • Change the rate to one which is much lower than the patients native rate
  • Increase the sensitivity value until no cardiac activity is sensed
  • Now, keep decreasing the sensitivity until the pacemaker senses every p-wave or QRS interval.
  • This minimal sensitivity value is the sensitivity threshold.
  • most of the time, you tend to leave the sensitivity turned down to half of the sensitivity thresholdto ensure that the cardiac electrical activity will be sensed even if the electrode tip overgrows with filth.
  • If you turn the sensitivity value down any more than that, you risk oversensing. Oversensing is described in greater detail elsewhere; briefly, it is an inappropriate inhibition of pacing in response to some sort of trivial non-cardiac signals, like the friendly hum of the nearby microwave.
While connected to the pacemaker, the patient suddenly drops his blood pressure and heart rate.
This 12-lead ECG is printed out. How do you interpret this?

CHB

Complete heart block

No evidence of pacing spikes

How would you troubleshoot the pacemaker in this situation?

Start with the box.

  • Is it even on?
  • Is the battery dying?
  • Are the wires detached from the pulse generator?
  • Are the leads connected?
  • Was the temporary pacing wire pulled out in course of a recent pressure area care?
  • Is the electrodes displaced? Is the transvenous electrode tip wiggling uselessly in the venticle?
  • Is there any weird twitching in the chest wall muscles of the patient? Is the ventilator demonstrating some bizarre sawtooth pattern, suggesting that the diaphragm is being paced?

Ok, so the hardware is intact. if there is output failure, its not because of the leads or the battery. Move on to the software.

First check the sensor threshold.

  • Put the pacemaker in a VVI, AAI or DDD mode.
  • Change the rate to one which is much lower than the patients native rate.
  • Observe the sense indicator.
  • Keep increasing the sensitivity.
  • Find the sensitivity maximum - where the pacemaker is picking up NONE of the endogenous electrical activity.
  • Now keep decreasing the sensitivity.
  • Find the sensor threshold - where the sensor picks up EVERY endogenous electrical event (i.e. no pacing spikes are visible)

Crank the sensitivity setting up to double the sensor threshold.

This should take care of oversensing as a cause of pacing failure.

Alternatively, as the college recommend in Question 2 from the first paper of 2016,  you can simply set the pacemaker to VOO mode. No sensing =  no oversensing.

Now, check the output threshold.

  • Set the pacemaker well above the native rate.
  • Start reducing the output.
  • Find the capture threshold - where a QRS complex no longer follows each pacing spike.

Crank the output to double the capture threshold.

The patient resumes pacing and awaits PPM insertion.
On Day 3, haemodynamic instability again becomes a problem.
The following rhythm strip is printed for you to review. How do you interpret this?

failure to capture

Failure of ventricular capture

The output is already near-maximal. What additional steps could you take to improve capture?
  • Roll the patient to one side, and then another. Sometimes this influences the position of the transvenous pacing wire tip just enough to get you some capture.
  • Reverse the leads. Sometimes this works, but logically - it shouldn't.
  • Convert to unipolar pacing. Attach the negative lead to the positive electrode, and the negative lead to the subcutaneous tissue of the chest.
  • Give up. Time to pace externally while waiting for another wire to be floated, or the epicardial leads to be resited.
The patient goes for an urgent PPM insertion. His St.Jude model is set to DDD pacing.
What are the advantages and disadvantages of this mode?

Advantages:

  • AV synchrony is preserved
  • "Pacemaker syndrome" is thus avoided
  • Advantageous in patients with normal atrial activity and a dysfunctional AV node
  • Versatile mode, with hemodynamic

Disadvantages:

  • Two leads required
  • Bundle of His is bypassed
  • Possibility of "endless loop" tachycardia
  • Increased risk of perforating the thin atrial wall
The patient's daughter has done some Googling and asks you whether cardiac resynchronisation therapy would benefit her father. What is the rationale for CRT?
  • In brief, if you have LBBB, the electrical activation of the lateral wall of the LV can be significantly delayed, when compared to the activation of the RV and the septum
  • Dyssynchronous electrical activation results in dyssynchronous contraction, which is mechanically inefficient.
  • CRT restores synchrony to ventricular contraction in patients with severe heart failure.
  • The potential benefit is improved cardiac output, without much (or any) increase in myocardial oxygen consumption.

Evidence?

  • The bottom line is that CRT improves NYHA grade, and it may improve mortality.
  • There is strong evidence that CRT reduces mortality and hospitalisation  (i.e. it is superior to AICD or medical therapy).
  • CARE-HF (2005) demonstrated improved symptoms and reduced risk of death from 20% to 30% (over a 2-year period) in patients with NYHA III or IV stage of heart failure.
  • Critics comment that this may be due to the built-in AICD function and the prevention of sudden cardiac death or arrhythmia-induced heart failure by these devices.
What are the guideline indications for CRT?
  • To benefit, one must have LBBB, a wide QRS, and an LVEF less than 35%.
  • Generally, only about 5-10% of heart failure patients will benefit
  • There is a "heterogeneity of effect" in patients  who do not meet the recognised criteria (read: it does them no good)

Disclaimer: the viva stem above may be an original CICM stem, acquired from their publicly available past papers. Or, perhaps it is a slightly altered version of the original CICM stem. Or, it is a completely original viva stem, concocted by the monstrously amoral author of Deranged Physiology for nothing more than his own personal amusement. In either case, because the college do not make the main viva text or marking criteria available, almost everything here has been confabulated. It might sound like a plausible viva and it could be used for the purpose of practice, but all should be aware that it does not represent the "true" canonical CICM viva station. 

References

Reade, M. C. "Temporary epicardial pacing after cardiac surgery: a practical review." Anaesthesia 62.3 (2007): 264-271.

Reade, M. C. "Temporary epicardial pacing after cardiac surgery: a practical review: Part 2: Selection of epicardial pacing modes and troubleshooting."ANAESTHESIA-LONDON- 62.4 (2007): 364.

Gammage, Michael D. "Temporary cardiac pacing." Heart 83.6 (2000): 715-720.

Abu-Omar, Yasir, Lorenzo Guerrieri-Wolf, and David P. Taggart. "Indications and positioning of temporary pacing wires.Multimedia Manual of Cardio-Thoracic Surgery 2006.0512 (2006): mmcts-2005.

Harrigan, Richard A., et al. "Temporary transvenous pacemaker placement in the Emergency Department." The Journal of emergency medicine 32.1 (2007): 105-111

Brignole, Michele, et al. "2013 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy." European heart journal (2013): eht150.

Jarcho, John A. "Resynchronizing ventricular contraction in heart failure." N Engl J Med 352.15 (2005): 1594-1597.

Cleland, J. G., et al. "Cardiac Resynchronization-Heart Failure (CARE-HF) Study Investigators. The effect of cardiac resynchronization on morbidity and mortality in heart failure." N Engl J Med352.15 (2005): 1539-49.