Viva 8

Created on Thu, 06/04/2015 - 00:36
Last updated on Wed, 02/07/2018 - 03:55

You are working as a consultant in a regional ICU. You have instructed your registrar to insert a right IJ central central line into a patient with poor venous access, for TPN administration. The patient day 10 in ICU,  recovering from abdominal surgery complicated by ileus. Her background consists of COPD and CCF.

The registrar calls you for help near the end of the procedure.

When you arrive, this is the patient's monitor screen.

Describe how you will approach this situation.
 

This patient is peri-arrest

1) Ensure personal safety

2) Perform a basic peri-arrest primary survey

  • Immediate assessment to diagnose cardiac arrest
    • Are they awake?
    • If they appear unconscious, shake them and ask "Are you alright?"
    • If they are unresponsive, look listen and feel for respiratory effort.
    • If the patient is unconscious, unresponsive, and is not breathing, call for help and start CPR.
      Otherwise, move on with the structured approach to prevent cardiac arrest
  • Airway:
    • Assess patency: best done by interrogating the patient. If he provides coherent answers to your questions, his ABCs are unlikely to be desperately compromised. If he does not, one should secure his airway - initially usig unsophisticated techniques (jaw thrush, chin lift), progressing through airway adjuncts to intubation as needed.
    • Look for presence of vomit or foreign body
    • Prepare to progress to intubation
  • Breathing
    • Observe respiratory rate
    • maintain oxygenationintially with high flow oxygen via tight-fitting reservoir mask. A high flow nonrebreather mask not only delivers around 75% FiO2, it also allows one to assess respiratory function by observing the expiratory fogging of the clear plastic, and one can hook up an end-tidal capnometer to it to detect expired CO2.
    • progress to bag-mask ventilation if respiratory arrest occurs
    • Auscultate the chest, percuss it, palpate for surgical emphysema
    • Investigate with ABG and urgent CXR
    • Specific differentials to consider before moving on with the survey:
      • Massive PE (distended neck veins, cyanosis, tachycardia and hypotension)
      • Acute severe asthma (silent hyperexpanded chest, the hint of wheeze)
      • Tension pneumothorax (unequal air entry, deviated trachea, hyper-resonant chest)
      • Massive haemothorax or effusion (unequal air entry, deviated trachea, dull percussion note over the hemithorax)
      • Pulmonary oedema (pink frothy sputum, coarse gurling creps)
  • Circulation
    • Ensure large-bore IV access
    • Measure the blood pressure non-invasively and attach ECG leads for monitoring
    • administer IV fluids as bolus
    • administer readily available vasopressors, eg. metaraminol in order to maintain cerebral perfusion
    • assess for sources of bleeding
    • ABG or FBC to assess Hb, and need for transfusion
    • rapid bedside TTE to assess cardiac chamber volume and contractility
    • Specific differentials to consider before moving on with the survey:
      • Extremes of hypovolemia (collapsed veins, empty chambers, slow capillary refill, dry mucosae, cool extremities, weak rapid pulse)
      • Haemorrhagic shock ( exactly as above but also deathly pallor)
      • Cardiac tamponade (distended neck veins, muffled heart sounds, electrical alternans on ECG)
      • Peri-arrest arrhythmia (eg. VT or SVT)
      • Severe sepsis (mottled skin, fever, hyperdynamic circulation with hypotension)
    • A fluid bolus would be an appropriate reaction in any case. A hand-operated pump giving set with a litre of crystalloid should be set up. Ideally, one should prepare for invasive arterial blood pressure monitoring.
  • Disability/neurology
    • Assess for signs of intracranial catastrophe by performing a brief neurological examination, including pupils and muscle tone/reflexes
    • Test BSL: ensure normoglycaemia
    • Specific differentials to consider before moving on with the survey:
      • Intracranial catastrophe (pupils, focal signs)
      • Seizure (increased tone, exaggerated reflexes, gaze deviation, clonus)
      • Extreme hypoglycaemia
      • Hyperglycaemic coma
      • Extremes of electrolyte derangement (eg. a sodium of 90 or 190)
      • Hepatic encephalopathy
  • Exposure/examination
    • Assess for sources of bleeding
    • Examine for features of anaphylaxis
    • Check temperature; ensure normothermia
What immediate investigations will you ask for?

Immediate investigations

  • ABG
  • CXR
  • FBC, EUC, CMP, LFT, group and screen, blood cultures (as well as any other relevant body fluid)
  • ECG

Investigations in the short-medium term

  • CTPA
  • CT of any specific suspicious cavity (abdomen, chest, brain)
  • TTE
  • random cortisol level, TFTs, etc (to exclude exotic causes of haemodynamic instability)
The bedside TTE yields these images. 

What is the main pathology here?

The findings are:

1) Very large pericardial effusion
2) Right ventricular compression.
Cardiac tamponade

The patient has likely developed cardiac tamponade during the insertion of the central line; one of the possible explanations is that the line tip or guidewire has perforated the right atrium.

What other clinical signs would you expect to find?
  • Hypotension
  • Elevated JVP /CVP (neck vein distension with inspiration- Kussmaul’s sign)
  • Muffled heart sounds
  • Tachypnoea
  • Exaggerated drop in diastolic CVP (Friedrich’s sign)
  • Absent y descent on CVP trace
  • Clinical signs of shock- decreased peripheral perfusion, slow capillary refill, oliguria, confusion.
What other signs would you expect to find on a more detailed echocardiogram?
The patient continue to deteriorate and the echo machine has malfunctioned. Describe your approach for a blind pericardiocentesis technique.
  • Raise the head of the bed 45° if the situation permits
  • Antibacterial prep and drape
  • Palpate the xiphisternum and ribs: that is your landmark.
  • There are three main approaches:
    • Subxiphoid approach: Insert needle just under the xiphoid, and advance in the direction of the left shoulder while aspirating.
    • Parasternal approach: Insert the needle perpendicular to the chest wall in the fifth intercostal space, just lateral to the sternum.
    • Apical approach: insert the needle in the intercostal space below and 1 cm lateral to the apex beat, aimed toward the right shoulder.
  • Withdraw fluid until cardiac output improves
  • Advance guidewire and dilate over it.
  • Advance pigtail catheter over guidewire, and suture in place

The college answer also suggests one connect  an ECG lead (one of the chest leads) to the base of the needle  and watch the ECG to look for a change  in  the  QRS  morphology,   or  ST  elevation  if  the  needle  contacts  the myocardium.

What are the possible complications of pericardiocentesis?

Complications of pericardiocentesis include:

  • myocardial perforation
  • bleeding
  • pneumothorax
  • arrhythmia
  • acute pulmonary oedema (due to rapid drainage of periciardial fluid leading to excessive LV preload)
  • acute ventricular dilatation
Pericardiocentesis yields approximately 400ml of blood and the patient's haemodynamics improve. Shortly after the drain is placed, the patient becomes unresponsive.  
Describe your management to this situation.

1) Confirm cardiac arrest

2) Call for help

3) Commence BLS (CPR) as a sole responder until help arrives

  • 100 compressions per minute
  • Compression to a depth of 1/3rd of the anterior-posterior chest diameter
  • If airway is unprotected, 30:2 ratio of compressions to breaths
  • If intubated, asynchronous ventilation of 8-10 breaths per minute
  • Ensure the ETT is not malpositioned (chest examination, end tidal CO2 or calorimetry)

4) Once help arrives, commence ALS arrest algorithm

  • Apply defibrillator pads and charge defibrillator with CPR in progress
  • Perform a rhythm check, minimising interruption of compressions
  • If shockable rhythm, administer shock:
    • Then, adrenaline every 2nd rhythm check
    • Amiodarone after the 3rd shock (300mg)
  • If non-shockable rhythm, administer adrenaline 1mg.

5) Exclude treatable causes of cardiac arrest (4 Hs and 4 Ts).

The rhythm on the defibrillator is sinus tachycardia. What are the possible causes of this cardiac arrest?

For the majority of situations, being able to reason in terms of Hs and Ts is enough. These are the reversible causes. To repeat them again:

  • Hypoxia 
  • Hypovolemia 
  • Hyper/hypokalemia 
  • Hyper/hypothermia 
  • Tension pneumothorax 
  • Tamponade 
  • Toxins 
  • Thrombus 
ROSC is achieved after 2 minutes of CPR. 

During resuscitation, the staff noticed that the new central line lumens have remained uncapped. How could this have contributed to the cardiac arrest?

A gas embolus could have occurred, particularly after the central venous pressure load was relieved by pericardiocentesis

What are the clinical features and complications of gas embolism?
  • Tachypnoea and dyspnoea: If the collection of emboli in the pulmonary circulation was slow, when about 10% of the pulmonary circulation is filled with gas it tends to produce what Palmon et al call a "gasp reflex", i.e. the sensation of breathlessness.  This can make things worse (eg. each deep panic-driven breath entrains more gas into the carelessly unclamped CVC lumen).
  • Hypoxia due to shunt: There is usually some hypoxia associated with a venous gas embolism, and this is due to some sort of worsened shunt. Blood does not flow through the air-filled pulmonary vessels; ergo all blood flow is directed into airless vessels, and there may not be enough time to oxygenate all of it on the way though the remaining functional pulmonary circulation. In short, a V/Q mismatch develops where Q is the problem.
  • Shunt-related changes in the end-tidal CO2: That is to say, just as in the case of pulmonary embolism there will be an abrupt drop in EtCO2, resulting from the sudden increase in pulmonary dead space.
  • Cardiac murmur: A characteristic "mill-wheel" murmur may be audible, but is a late sign - by the time your patient is mill-wheeling they would be peri-arrest. 
  • Gas bubbles in the retina, on fundosccopy
  • ECG changes associated with gas embolism: There is no pathognomonic wave here, but ECG will be different-looking. According to a case report by Cooney et al (2011), changes may include tachyarrhythmias, AV block, right ventricular strain (right axis deviation, T-wave inversion and ST depression in anterior and inferior leads), poor R-wave progression and ST segment changes. 
  • Increased pulmonary arterial pressures: It would seem strange that the right ventricle might experience increased resistance given that the obstruction to flow consists of nice soft air, but indeed the PA pressure tends to rise.
  • Paradoxical embolisation: This can happen when the right sided pressure gets too high. Either a previously dormant foramen will open, or the air will penetrate into the left sided ot the circulation via pulmonary capillaries. Either way, systemic arterial emboli will result. Apart from the brain, probably the next most horrible site of embolisation would be the coronary arteries. 
  • Characteristic TOE findings Palmon et al list investigations for gas embolism, in order of their sensitivity. TOE turns out to be the best, demonstrating classical echogenic bubbles. This technique can detect as little as 0.02ml/kg of gas. The added bonus is being able to assess for paradoxical embolism.
How would you manage a gas embolism?
  • Disconnect the nitrous oxide. This gas is notorious for collecting in air-filled cavities. N2O will rapidly diffuse into trapped air bubbles and increase the size of the embolus.
  • Put the patient in a flat (supine) position.  A head-down position was once recommended, for two main reasons.  Firstly, any air bubbles in the arterial circulation should spare the brain and bubble up into the gut and legs. Secondly, the gas should collect in the RV apex, where it will hopefully stay - the base of the RV will still be full of blood and the RV will still have something to pump. 
    In actual fact, this turns out to be complete bullshit. The buoyancy of gas bubbles is not sufficient to counteract blood flow propelling such bubbles toward the head, so you won't save the brain this way- but you certainly will exacerbate cerebral oedema. 
  • Aspirate the gas using a right atrial catheter (or a long CVC, or a PA catheter).
  • Crank the FiO2 to 100%. Apart from being a stereotyped knee-jerk response to hypoxia, this manoeuvre helps to decrease the volume of the gas bubbles, provided atmospheric air is the embolic source. The administration of oxygen as the sole respiratory gas will lead to an increased gradient for nitrogen to exit the air bubbles. An excellent article by Van Liew et al (1992) discusses this phenomenon in luxurious detail. 
  • Hyperbaric oxygen therapy may be useful, particularly for paradoxic cerebral air embolism. The aim is to decrease the size of the bubbles by creating a nitrogen gradient (as above), but also to improve the oxygenation of ischaemic tissue (i.e. the brain). R.E. Moon (2014) discusses the use of hyperbaric oxygen in this setting; apparently the otcome is better with this "recompression" therapy. apparently, it is indicated even after significant delay, and even when there no apparent air in the CT of the brain.
  • Antiepileptic therapy - specific for cerebral gas embolism; these people are prone to seizures.

The original college viva text was as follows:

"Procedure station was about central venous access.

Areas of weakness identified by examiners:

Inability to clearly describe anatomical relationships"

As you can see, much modification has taken place.

Disclaimer: the viva stem above is the original CICM stem, acquired from their publicly available past papers. However, because the college do not make the rest of the viva text or marking criteria available, the rest has been confabulated. It sounds like a plausible viva and it can be used for the purpose of practice, but all should be aware that it does not represent the "true" canonical CICM viva station.