Viva 8

You have been asked to review a patient 4 hours post coronary artery bypass surgery who is increasingly inotrope dependent.

What common techniques and measurements are available to assess the adequacy of the circulation and cardiac output?

Techniques for the Assessment of Circulation

Clinical techniques Capillary refill Heart rate Temperature of the extremities Urine output Mental state Pressure-based techniques Non-invasive blood pressure Invasive blood pressure (arterial line) Central venous pressure Flow-based techniques Thermodilution cardiac output measurements Right heart (PA catheter) Trans-pulmonary (PiCCO) Trans-thoracic Echocardiography (TTE) Transoesophageal echo (TOE) Continuous oesophageal PW Doppler Transcutaneous Doppler

Static indices of fluid responsiveness LVEDVI, RVEDVI GEDVI ITBV Dynamic indices of fluid responsiveness Response to fluid challenge Passive leg raise Pulse pressure variation Stroke volume variation Assessment of circulatory efficacy Lactate measurements Central or mixed venous saturation Oxygen extraction ratio a-A CO2 difference Assessment of microcirculation Gastric tonometry Sublingual tonometry Microdialysis Experimental techniques Impedance cardiography

This also came up in Question 13.1 from the second paper of 2012.

Determinants of cardiac output and methods of its measurement were asked about in Question 2a, Question 2b and Question 2c from the second paper of 2000.

Cardiac output monitoring:

Technique of cardiac output monitoring	Advantages	Disadvantages
PA catheter	“Gold standard” of CO monitoring Easy to insert Interpreter-independent	Risk of vascular access Unreliable with septal defects or tricuspid regurgitation Thrombotic complications Potential for valve damage
PiCCO	Easy to insert Interpreter-independent	Risk of vascular access Unreliable with septal defects , tricuspid regurgitation or arrhytmia Invalidated by rapid changes in vascular tone
Transthoracic Doppler	Non-invasive	Interpreter-dependent Poor reproducibility in serial assessments Depends heavily on image quality
Oesophageal Doppler	Minimally invasive	Positional; risk of gastric or oesophageal perforation
SvO2 measurments	Easy to insert  Interpreter-independent	No information on  regional oxygen extraction Assumptions regarding cardiac output
Pulse dye densitometry	Interpreter-independent	Difficult to perform Specialized equipment required Exposure  to dye may be undesirable  Studies of validity give conflicting results
Bioimpedance cardiography	Non-invasive	Thus far not validated for clinical use

Your patient already has a central line. How could you use this device to monitor the efficacy of the circulatory system?

• CVP (crude and dodgy)
• Central venous saturation (ScvO₂)
• Arteriovenous CO₂ gap
• Arteriovenous lactate gap
• Oxygen extraction ratio

What is the oxygen extraction ratio? How is it calculated?

• In summary, the oxygen extraction ratio is  VO₂ / DO₂. 
  • VO₂ = CO ×(CaO₂ - CvO₂)  ...this is the global oxygen consumption
  • DO₂ = CO ×CaO₂ ...this is the global oxygen delivery.
• In order to calculate this, one requires the cardiac output and the oxygen content of the blood.
• The oxygen carrying capacity of blood remains fairly stable in ICU patients
• So, really, the only variable which actually varies is the mixed venous saturation. Thus the O₂ER  equation can be simplified as follows:
  O₂ER  = (SaO₂-SvO₂) / SaO₂
  Or even more simply,
  O₂ER  = 100% - SvO₂ (in percent)
  (assuming that the arterial saturation is close to 100%).

What is a normal oxygen exraction ratio? What is the range of normality?

The normal ratio is 0.2-0.3, which corresponds to an ScVO₂ of 70-80%.

At a certain O₂ER (probably around 60-70%) probably represents some sort of critical level; studies of dying ICU patients have revealed that lactate starts rising at a critical SvO₂ value of around 40%.

You calculate an O₂ER of 45%. What are the causes of such a low extraction ratio?

Inadequate oxygen delivery:

• Hypoxia
• Anaemia
• Blood flow insufficiency: shock states of all sorts

Increased oxygen consumption:

• Increased muscle activity:
  • Exercise, including respiratory effort
  • Shivering
  • Seizures
• States of inflammation, eg. sepsis
• Increased metabolic rate:
  • Hyperthermia
  • Hyperthyroidism
  • Catecholamine excess
  • Response to massive injury or burns

Abnormal circulation:

• Right-to-left shunt (cyanotic defect)
• Arteriovenous malformations
• Portosystemic shunts (in liver disease)

Measurement artifact:

• Post-collection error in the VBG (prolonged sample-to-machine transit time)

The cardiac surgeon laughs derisively at your use of ScvO2. What is the difference between central venous and mixed venous saturation?

• The relationship is different in health and disease.
• Oh's Manual specifies that under normal physiological conditions central venous saturation (ScvO₂) is 2-3% lower than mixed venous oxygen saturation (SvO₂).
• In pathological states, ScvO₂ is often higher than SvO₂ by about 5%
• Why is this the case?
  • SvO₂ can be abnormally depressed under the following circumstances:
    • Increased myocardial oxygen extraction, eg. hyperdynamic cardiac failure or coronary insufficiency
    • Shock (increased splanchnic oxygen extraction)
  • ScvO₂ can be abnormally increased:
    • Decreased cerebral metabolism:
      • Hypothermia
      • Anaesthesia
    • Decreased upper body metabolism
      • Paralysis

The surgeon insists you use this device for haemodynamic monitoring.
What is this device? What are its main features?

(ideally, the candidate should be offered an actual PAC as a prop to fiddle with. The depicted catheter is an el cheapo Edwards product, which expired from neglect. Good quality catheters with heating filaments and SvO₂ probes might be available where you are)

The anatomy of the PA catheter came up in  Question 28.1 from the first paper of 2011.

What are the indications for the use of this device?

• Cardiac output measurement especially in a patient with arrhythmia or aortic balloon pump, where PiCCO cant be used
• Unequal right and left ventricular failure
• Complex hemodynamic instability, some combination of obstructive, distributive, cardiogenic and hypovolemic shock
• To differentiate cardiogenic pulmonary edema from non-cardiogenic
• To guide use of vasopressors, inotropes, fluids and diuretics – when the patient has a hemodynamic problem combined with pulmonary oedema and ventricular dysfunction.

• To titrate pulmonary antihypertensives in ARDS (like nitric oxide and prostacyclin)

What are the complications of the use of this device?

Same as CVC:

• Perforation of SVC
• Haemothorax, pneumothorax
• Atrial fibrillation

Unique to PA catheter

• Ventricular Arrhythmia
• Thromboembolic events (the catheter is a nidus for clot formation)
• Mural thrombi in the right heart (up to 30%)
• Air embolism from ruptured balloon
• Pulmonary infarction
• Endocarditis of the pulmonary valve ( 2%)

Right bundle branch block

• If you already have LBBB, this causes complete heart block
• If you are lucky, it is a transient phenomenon and you only need to pace them transcutaneously for a brief period. If you are unlucky, you have injured the AV node, and the patient needs prolonged transvenous pacing

Knotting on structures or on itself ( ~ 1%)

• If it has gone into the right ventricle by 25-30cm and its still not in the pulmonary artery, you start to worry

Damage to the valves or the heart

•  Never pull the catheter back with the balloon inflated! You could tear the valve leaflets
• The RV can be perforated, particularly a dilated weak-walled RV
• The RA can be perforated (perhaps even more easily)

Pulmonary artery rupture: 0.2% risk,  30% mortality

• Risk factors: pulmonary hypertension, mitral valve disease, anticoagulants and age over 60

Can you describe the process of its insertion?
What major changes take place in the pressure reading?

• The introducer sheath goes in first.
• Before the PA catheter is threaded in, the distal lumen is connected to a CVP transducer, so the pressure wave can be observed.
  • The pressure here will be 1-6mmHg.
• Once you are in the  right ventricle:
  • The systolic pressure here should be between 15 and 30mmHg.
  • The diastolic should be same as right atrial pressure, about 1-6mmHg (makes sense given that the right ventricle fills from the right atrium).
• As soon as you are in the RV, and are seeing the pulse waveform, you can inflate the balloon with air. The volume is 1.5ml.
• Past the pulmonary valve, one can now see the PA waveform, which resembles the waveform of any other artery.
  • At this stage the diastolic pressure rises to about 6-12mmHg
  • Systolic pressure should be no higher than 25 or so
  • Mean pressure should be around 9-18 mmHg
• The catheter with the inflated balloon is advanced further, until the PA waveform disappears, and a venous-looking waveform appears.
• This is the wedge waveform.
  • The pressure here should also be 6-12 mmHg.

Which direct measurements can be made from the PA catheter?

• Core temperature
• RA pressure
• RV pressure
• PA pressure
• PA wedge pressure
• Mixed venous saturation

On which assumptions do we rest our confidence in the validity of pulmonary artery wedge pressure as a measure of preload?

We assume that:

• Pulmonary artery wedge pressure is the same as left atrial pressure
• Left  atrial pressure is the same as left ventricular end-diastolic pressure
• Left ventricular end-diastolic pressure is a good reflection of LV end-diastolic volume
   

How can you confirm that the catheter is in correct position?

To maintain a column of blood between the pressure transducer and the left atrium, the balloon has to be below the atrium. This means you have to send the catheter tip into Wests Zone 3 when you are floating it.

This should happen naturally because Wests Zone 3 normally enjoys higher blood flow.

Tests which suggest appropriate Zone 3 positioning of the PAC:

• On lateral CXR, the tip of the catheter is at or below the left atrium
• Respiratory variation of PAOP is < 50% of the static airway pressure (peak – plateau)
• Change the PEEP: PAOP changes by 50% of the change in PEEP
• The PAWP is less than the PA diastolic pressure
• The PAWP contour has recognizable a and v waves; in Zones 1 and 2 it is unnaturally smooth.
• Wedge PO2 minus Arterial PO2 = 19mmHg
• Arterial PCO2 minus Wedge PCO2 = 11mmHg
• Wedge pH minus Arterial pH = 0.008

• On the Xray, the tip should appear 3 -5 cm from the midline, no more than 2cm from the hilum.
• It should be INFERIOR to the LA position.

Under which circumstances would the wedge pressure be higher than LV end-diastolic pressure?

Pretty much anything that results in an obstruction (or reversal) of forward flow from the pulmonary circulation into the left ventricle will result in a PAWP higher than the LVEDP.

• Mitral stenosis (gradient across the mitral valve is high, LA pressure is increased)
• Atrial myxoma (same reason)
• Mitral regurgitation (large v waves interfere with wedge measurement, and LA pressure is high)
• Pulmonary fibrosis (obstruction to venous flow)
• Inappropriate placement (eg. into a high Wests zone)
• High PEEP
• High Auto-PEEP

Can you describe how you would perform a manual thermodilution measurement?  What is the underlying physiological basis of  this technique?

• A bolus of 5-10ml cold 5% dextrose into the right atrium should decrease the temperature in the pulmonary artery.
• The rate of blood flow is  inversely proportional to the change in temperature over time
• Thus, the mean decrease in temperature is inversely proportional to the cardiac output.
• The Stewart-Hamilton Equation describes this relationship
• The higher the cardiac output, the faster he blood flow and the shorter and steeper the thermodilution curve. In low cardiac output, the curve is slurred and lazy. Even more so in tricuspid regurgitation.

Correct technique:

• You should take measurements in expiration.
• You have to take a mean of 3 measurements.
• The mean has to be 15% different to the previous mean, otherwise it is within the margin of error.
• The thermodilution cardiac output can vary by 10% from measurement to measurement without any change in the condition of the patient

Practical problems:

• Too much injected cold stuff causes underestimation of cardiac output.
• Too little injected cold stuff causes overestimation of cardiac output.
• Room temperature injectate  produces less accurate readings, but is safer.
• Very cold injectate (0-4 degrees) is more accurate, but can induce bradycardia and decreased cardiac output.

What patient factors might cause an inaccuracy of thermodilution cardiac output measurements?

This came up in Question 19 from the second paper of 2007.

In summary:

• Catheter is in the wrong position
• The thermistor tip is up against the wall
• The respiration is erratic
• There is an intracardiac shunt
• Tricuspid regurgitation
• Cardiac arrhythmia
• Rapid infusion happening via the IJ line
• Abnormal haematocrit
• Slow injectate delivery
• Injectate not cold enough, or not enough of it

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.