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.
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:
Anyway, the causes of low cardiac output and some investigations/observations:
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."
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 |
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:
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:
The following abnormalities are apparent:
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.
Denault et al (2010) offer an excellent article on this topic; the following list is derived from their Figure 5
IV pulmonary vasodilators:
Inhaled vasodilators:
(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
Mechanical decompression
There is:
There is a great article on this (Barker et al, 1989). In brief:
Nitric oxide is genotoxic. It damages DNA in a vicious, direct fashion. On top of that, the following adverse effects have been reported:
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.
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.