Viva 6

A 53-year-old male returns from theatre on high dose inotropic support following Aortic Valve Replacement and Coronary Artery Bypass Graft x 4. He had a long pump time of 252 minutes and pre and post-op left ventricular function are very poor with global hypokinesis.
 
There are no surgical issues. His cardiac index is 1.6 L/min/m2.
His urine output for the last hour is 2 mL and his serum HCO3- is 15 mmol/L with a lactate of 8 mmol/L.
He is ventilated in a mandatory mode with FiO2 = 0.85 & PEEP 15cmH20.

What could be the cause of his low cardiac output? What features of clinical examination and monitoring would you look for?

This is organised in a structure which follows answers to SAQs on the management and assessment of unstable post-pump patients; these were organised in terms of the variables which affect cardiac output, rather than in the more traditional approaches. The trainees may try to organise their thinking in a number of different ways, all of which would be legitimate.

Examples may include:

  • A systems-based approach (eg. cardiovascular causes, infectious, drug-related, endocrine, etc)
  • An A-B-C-D-E approach (from airway problems, to respiratory, etc)

Anyway, the causes of low cardiac output and some investigations/observations:

  • Preload-related: underfilled, obstructed or in tamponade
    • CVP
    • PCWP
    • Pulse pressure variation ("swing" in the arterial trace)
    • History of extensive blood transfusion or poorly controlled ooze intraoperatively
    • High chest drain output (>200ml per hr)
    • CXR evidence of pneumothorax
    • TTE evidence of RV dilatation (PE)
  • Afterload related: vasoconstricted or vasodilated
    • SVRI
    • PVRI
    • Clinical examination (eg. cool extremities, slow cap refill)
    • Temperature (ie. very cold after bypass)
    • Pre-op cultures positive, eg. UTI or LRTI
    • History of ACE-I use
  • Contractility impairement: myocardial stunning
    • Sluggish LV on TTE
    • Clinically, poor pulse amplitude and weak apex beat
    • Temperature (ie. very cold after bypass)
    • ECG changes suggestive of ischaemia
    • Severe metabolic acidosis (cardiodepressant effect)
    • Severe hypocalcemia (cardiodepressant effect)
    • History is important: was the AVR for AR or AS? Is there LVH or dilated cardiomyopathy?
  • Rate and rhythm related:
    • Bradycardia or tachycardia
    • AF
    • Ventricular extrasystoles
What are the possible complications of such a long bypass run?

This table is straight from the discussion section for Question 2 from the first paper of 2015:
"List the complications and their likely underlying mechanisms specifically related to cardiopulmonary bypass that may be seen in the Intensive Care Unit following cardiac surgery." 

Complications of Cardiopulmonary Bypass
Organised According to Organ Systems
Organ System Complication Aetiology
Respiratory Left lower lobe collapse Phrenic nerve neuropraxia, due to cold slush cardioplegia
Poor reinflation following restoration of circulation
Pulmonary hypertension Due to increased pulmonary vascular resistance (protamine)
Acute Lung Injury SIRS due to bypass circuit-associated complement activation
Cardiovascular Myocardial stunning Due to direct effects of cardiotomy and cardioplegia
Myocardial infarction Coronary graft ischaemia (air embolism)
RV dysfunction Due to pulmonary hypertension related to protamine
Arrhythmias Due to electrolyte disturbances and hypothermia
Heart block Due to hypothermia or direct conduction system trauma
Systemic MODS Hypoperfusion and end-organ ischaemia related to non-pulsatile flow and/or air/atheroma embolism
Neurological Stroke All thought to be due to the sluggish low-flow state following the recommencement of bypass, as well as due to air emboli microemboli and possibly microemboli from the bypass circuit itself
Watershed infarcts
Neurocognitive impairment
Electrolytes and
Endocrine
Hypothermia Due to intra-operative cooling and delayed re-warming
Hyperglycaemia Due to hypothermia-related insulin resistance
Due to circulating endogenous catecholamines
Electrolyte derangement Haemodilution
Renal Post-op diuresis "Cold diuresis" due to intra-operative cooling and delayed re-warming
Post-op renal failure Low flow, and thromboembolic events
Electrolyte derangement Haemodilution
Gastrointestinal Splanchnic ischaemia Low flow, and thromboembolic events
Hepatic dysfunction
Pancreatitis
Haematological Coagulopathy Due to consumption of clotting factors by the bypass circuit
Due to residual anticoagulation
Due to dilutional coagulopathy
Platelet dysfunction Due to antiplatelet agents, and due to the SIRS response
Anaemia Due to haemodilution and haemolysis
Haemolysis Due to mechanical destruction by the bypass pump, as well as due to MAHA and SIRS
Metabolic Hypothermia Due to intra-operative cooling and delayed re-warming
Hyperglycaemia Due to hypothermia-related insulin resistance
Due to circulating endogenous catecholamines
Immune Coagulation cascade activation Due to blood contact with non-biological surfaces and blood-gas interface
SIRS Due to complement activation by circuit components
Anaphylaxis A reaction to protamine
What options are available to improve this man’s tissue perfusion?

A good answer will be structured.

One good structure is to discuss the variables which affect cardiac output and which are open to manipulation. The cardiac output is clearly the thing that's broken here.

Thus:

  • Preload:
    • decrease PEEP to 5
    • Offer a fluid bolus, ~ 20ml/kg
    • At the bedside, look for US features of cardiac tamponade
  • Rate/rhythm
    • If he is paced, increase the rate to 80-90
    • Pace the atria, preferably
    • If he is in rapid AF, one may wish to slow him down and/or cardiovert him with amiodarone 
  • Contractility
    • Milrinone or levosmendan
    • Correct acidosis with some bicarbonate
  • Afterload
    • If the BP is high, reduce afterload using GTN / SNP
    • If BP is low, use some vasopressin (as it will be unaffected by the low pH); though noradrenaline is a valid alternative
  • Augmentation of cardiac output by mechanical means
    • IABP
    • LVAD
    • VA ECMO
  • Augmentation of oxygen carriage and consumption
    • Keep HB > 80
    • Re-warm the patient
    • Sedate and paralyse the patient with muscle relaxant, to reduce oxygen demand
How will you monitor the response to your interventions? What  are your therapeutic endpoints?

As far as specific parameters go, this is an evidence-free wasteland. One can choose any author from the literature and use their totally arbitrary numbers. For example, Ellis et al (1997) recommends in an authoritative non-EBM fashion to aim for the following parameters:

  • CI > 2.0 L/min/m2
  • CVP 8-10
  • PCWP 12-15 (16-20 if the LV is hypertrophied)
  • u/o >0.5ml/kg/hr
  • Lactate on a down-trend
  • MAP > 70
With inotropes commenced and PEEP rationalised, a thermodilution measurement is performed. Please interpret this data and explain how it affects your management.

The following abnormalities are apparent:

  • Tachycardia
  • Raised CVP (21)
  • Raised PCWP (24)
  • Raised PA mean pressure (42; normal is 9-18)
  • Low stroke volume (SV= 41;  normal is 60-100)
  • Low SVRI (1753; normal is 1950-2390)
  • High PVRI (554; normal is 255-285)
  • Satisfactory CI and SvO2

Overall, this gives the impression of a patient with predominantly right-sided cardiac pathology, with high pulmonary pressures and systemic vasodilation. The cardiac output is now satisfactory.

What are the potential causes of raised pulmonary pressures after cardiac surgery?

Denault et al (2010) offer an excellent article on this topic; the following list is derived from their Figure 5

  • Positive pressure ventilation with excessive pressures
  • Mechanical compression of pulmonary vessels by
    • Atelectatic lung or effusions
    • Distended abdomen
    • Enlarged mediastinal structures, eg. pericardial effusion
  • Underlying disease (pre-existing PHT)
  • LV dysfunction with increased LV end-diastolic pressures
  • Mitral regurgitation or stenosis
  • Pulmonary inflammation
  • Metabolic or respiratory acidosis
  • Hypoxia due to atelectasis
  • Protamine administration; excess noradrenaline
  • Pulmonary emboli
What are the options for managing this pulmonary hypertension?

IV pulmonary vasodilators:

  • Milrinone
  • Levosimendan
  • Intravenous prostacycline

Inhaled vasodilators:

  • Nitric oxide
  • Inhaled prostacycline

(the trainee should not be talking about sildenafil or bosantan here, as the patient is not going to absorb anything much orally and in any case immediate results are called for)

Metabolic manipulation

  • Correct acidosis
  • Ensure normocapnia and normoxia

Mechanical decompression

  • Decrease PEEP
  • Drain effusions/pneumothoraces
The department has only nitric oxide available. Can you explain its mechanism of action?
  • Nitric oxide is a potent vasodilator
  • It inhibits vasoconstriction by increasing the amount of cyclic GMP (cGMP) in the cytosol,
  • This decreases the amount of cytosolic calcium ions available to sustain contraction
What form does it come in? What are the pharmacokinetics of inhaled nitric oxide?
  • The gas comes in a pressurised cylinder, under a brand name "INOmax".
  • It contains 99.92% nitrogen and only 0.08% nitric oxide, or 800 parts per million (ppm).
  • The highest concentration you would ever use is about 80ppm, which corresponds to a gas mixture of 90% whatever, and 10% Inomax.
  • Nitric oxide is rapidly absorbed into the systemic circulation through the lungs
  • In the blood it undergoes some significant modifications:
    • It reacts with lung water, becoming nitrite (which reacts with oxyhemoglobin and generates methaemoglobin and nitrate)
    • It combines directly with oxyhaemoglobin, with the same results.
    • If it encounters hypoxic blood, it can combine with deoxyhaemoglobin to create nitrosyl-haemoglobin, which then rapidly becomes methaemoglobin when it contacts oxygen.
    • In all cases, it generates methaemoglobin and nitrate
What are the contraindications for the use of inhaled nitric oxide?
  • Left ventricular failure: NO seems to cause lots of adverse effects in this group of patients- particularly, pulmonary oedema. In fact, halfway through one study, the investigators had to start excluding CCF patients from the trial because of these effects.
  • Left to right shunting: NO will decrease the pulmonary (and thus the RV) pressure, increasing the amount of blood shunted via a septal defect.
  • Uncontrolled haemorrhage: Though there is no human evidence, in animal studies NO had been shown to increase bleeding times.
  • Existing methaemoglobinaemia: obviously, it will get worse. 
Several hours after commencement of inhaled nitric oxide, the nurses complain that the patient's saturation remains very low (~ 85%) on 100% FiO2. They have performed the following ABG. Please interpret it and explain the major abnormalities

There is:

  • Mild acidaemia
  • Normocapnea
  • Normal normal oxygen saturation (99%) contrary to the pulse oximeter reading - in fact, you could safely come down on the oxygen
  • Mild lactic acidosis
  • Methaemoglobinaemia (FMetHb is 28.8%)
Can you explain why the pulse oximeter reading is affected in this scenario?

There is a great article on this (Barker et al, 1989). In brief:

  • Oxygen saturation is the ratio of reduced haemoglobin to oxyhaemoglobin
  • Reduced haemoglobin and oxyhaemoglobin absorb different wavelengths;
    • Reduced Hb absorbs red light (660nm)
    • Oxygenated Hb absorbs infra-red light (940nm)
  • The pulse oximeter only uses these two wavelengths to calculate a red/infrared absorption ratio, or R value
  • The absorbance spectrum of methaemoglobin for red and infrared is very similar, and the R value is therefore close to 1 (which in the pulse oximeter look-up table corresponds to a saturation of around 82%
  • Thus, increasing methaemoglobin levels will result in a pulse oximeter reading which trends towards 82%. A plateau is reached at an FMetHb of around 30-35%.
Apart from methaemoglobinaemia, what are the other adverse effects of inhaled nitric oxide?

Nitric oxide is genotoxic. It damages DNA in a vicious, direct fashion. On top of that, the following adverse effects have been reported:

  • Hypotension (maybe some of it does leak into the systemic circulation, or maybe this the effect of depressed LV function
  • Rebound hypoxia after abrupt withdrawal
  • Thrombocytopenia (in as many as 10% of patients)
  • Increased susceptibility to pulmonary infections probably due to NO2 formation and associated lung injury. 
 
 

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

Eillis, Myra F. "Low cardiac output following cardiac surgery: critical thinking steps." Dimensions of Critical Care Nursing 16.1 (1997): 48-55.

Edwards: normal hameodynamic parameters chart

Denault, André, et al. "Pulmonary hypertension in cardiac surgery." Current cardiology reviews 6.1 (2010): 1-14.

Barker, Steven J., et al. "Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: a human volunteer study." Anesthesiology105.5 (2006): 892-897.

Tremper, Kevin K. "Pulse oximetry." CHEST Journal 95.4 (1989): 713-715.

von Kompen, E. J. "Spectrophotometry of hemoglobin and hemoglobin derivatives." Advances in clinical chemistry 23 (1983): 199.

Barker, Steven J., Kevin K. Tremper, and John Hyatt. "Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry." Anesthesiology 70.1 (1989): 112-117.