The 5 top anaesthetic complications in medical patients (and how to fix them!)
Tell me if I’m wrong, but I feel like we nurses fall into two camps: team ‘I love anaesthesia!’ and team ‘I don’t like +/- am a little afraid of anaesthesia’. And for a long time, I fell into the latter.
Now don’t get me wrong, I am not saying anaesthesia is my favourite part of the job - and for a long time, I was terrified of it because I didn’t do enough of it (and because my patients are quite complicated, making their GA’s more complicated!)
In reality, though, knowing how to safely anaesthetise our medical patients, and how each of their different diseases impacts our anaesthetic considerations, is an important part of medical nursing.
On top of knowing how to plan for and monitor our patient’s GAs, we also need to understand the common complications we can see during the anaesthetic, and how to manage these.
Today I’ll be sharing 5 anaesthetic complications we encounter in our medical patients, why they occur, and the steps you need to follow to troubleshoot them.
By the end of this post, you should have a better understanding of how to manage these complications, and feel more confident monitoring your patients!
1: Hypotension
Hypotension is a really common complication during anaesthesia. It’s defined as a systolic BP of less than 80-90mmHg, a mean BP of less than 60-70mmHg, and a diastolic BP of less than 40mmHg.
Ideally, we want to be measuring blood pressure routinely in every anaesthetised patient - especially our patients with comorbidities or illnesses such as our medical patients!
As well as monitoring blood pressure, we also want to assess perfusion by assessing things like mucous membrane colour, capillary refill time and peripheral pulse quality checks.
What impacts blood pressure under GA?
Lots of things affect blood pressure under anaesthesia, including:
Premedication drugs
Induction agents
Inhalant anaesthetics
Hypothermia
Hypoglycaemia
Diseases affecting cardiovascular/volume status (e.g. anaemia or hypoproteinaemia)
Haemorrhage
Many of our medications cause varying changes to cardiac contractility and vascular resistance. These things will both affect blood pressure significantly.
If hypotension is noted under GA, we see a decrease in perfusion to organs and tissues. This can result in complications such as acute kidney injury, for example, if the kidneys do not receive sufficient blood flow for long enough.
So how do we avoid hypotension?
We want to avoid hypotension by developing a balanced anaesthetic plan, using multimodal techniques.
This means we’ll use a lower dose of various anaesthetic agents, minimising their cardiovascular effects. Local and regional anaesthetic techniques are also fab additions here, meaning we can use less sedation, and lower volumes of volatile agents.
And how do we manage hypotension?
The steps I would use to troubleshoot hypotension are:
Assess anaesthetic depth. Can we reduce our volatile agent? If the patient seems painful, could we give them more analgesia instead of increasing the gas, for example?
Assess fluid balance. Is there a complication such as a bleed causing a sudden drop in blood pressure, for example? If the patient is hypovolaemic, we need to address this with volume resuscitation.
If your patient’s volume status is normal and they’re appropriately anaesthetised, do we need to think about medications to address their hypotension? There are several we can use, depending on the reason for their hypotension. These include:
Anticholinergics: such as glycopyrrolate
Sympathomimetics: such as ephedrine
Inotropes: such as dobutamine, used to increase cardiac contractility
Vasopressors: such as noradrenaline, used to increase systemic vascular resistance by causing vasoconstriction
2: Tachycardia
What's the first thing you think of when your patient is tachycardic under anaesthetic? Too light, right?
Well, the answer is not always.
Yes, often it indicates our patient isn’t adequately anaesthetised. But often it can be seen as part of our patient’s disease process or their procedure (e.g. if you’re doing anything to an adrenal gland in theatre, you might well see some scary tachycardia!), or as a consequence of a drug we’ve given (such as alfaxalone, ketamine, glycopyrrolate, atropine or terbutaline).
Things to think about before you adjust your volatile agent are…
Pain: are we now doing something the patient finds uncomfortable? If so, treat the pain, rather than increasing the gas - it might be time for some more analgesia (when did they have their premed?!), they might need a top-up, or we might need to think about giving other analgesics - e.g. paracetamol, or NSAIDs).
Hypoxaemia: is your patient hypoxaemic? If so, they may be tachycardic as they try and move their oxygen around the body faster. Check SpO2 (and, if needed, increase their oxygen), ensure your ET tube is not occluded, or treat the underlying respiratory disease (if one is present).
Hypovolaemia: has your patient just had a bleed? Or are they behind on fluids? If so, they’ll try and maintain their cardiac output by increasing their heart rate. Treat with crystalloid boluses and/or blood products, depending on what your patient has lost - and keep a close eye on heart rate, blood pressure and mucous membranes/CRT to assess the patient’s response!
Hypercapnia: if your patient’s ETCO2 is high, they might be tachycardic as they try and pump that CO2 to the lungs faster for elimination. If that’s the case, troubleshoot the ETCO2 - either by treating the cause of the hypoventilation, increasing your fresh gas flow, or minimising dead space in your circuit, for example.
3: Anaesthetic Arrhythmias
We can see several different arrhythmias in our medical patients under anaesthesia, including:
Sinus tachycardia (aka tachycardia)
Where the electrical conduction pathways through the heart are normal, but the heart beats too rapidly, e.g. in response to pain, or to compensate for hypovolaemia.
Sinus bradycardia (aka bradycardia)
Where the conduction pathways through the heart are normal, but the heart beats too slowly. This can be seen in response to cardiovascular depression from anaesthetic agents, due to hypovolaemia, or due to electrolyte abnormalities (e.g. hyperkalaemia)
Atrioventricular block (‘AV block’)
There are 3 different types of AV block - 1st degree, 2nd degree and 3rd degree. 1st and 2nd-degree AV blocks cause partial blocking of the electrical conduction through the heart, whereas 3rd-degree AV block results in complete heart block.
In AV block, the electrical signals from the atria cannot travel to the ventricles normally. Some forms of AV block can be caused by increased vagal tone, and certain medications (e.g. short-term AV block can be seen with alpha-2 agonists).
1st degree AV block has a P wave for every QRS complex, but the PR interval is longer as conduction is delayed.
2nd degree AV block can be divided into type 1 and type 2.
In type 1, the PR interval progressively increases with each heartbeat, until an impulse is not conducted and a QRS complex is missing.
In type 2, the PR interval is constant with intermittent missing QRS complex. This usually results in a repeating cycle of a missing QRS complex after every 3-4 P waves.3rd degree AV block is complete heart block, where there is no communication between the atria and ventricles. These patients have a junctional escape rhythm with random, narrow QRS complexes not associated with P waves. 3rd degree AV block is treated with pacemaker implantation.
Ventricular Premature Complexes (VPCs), AIVR and VT
VPCs occur when an abnormal electrical impulse arises from the ventricles, causing them to contract. They can occur as single complexes, in pairs or threes, or in runs.
They are usually caused by myocardial diseases, systemic diseases (e.g. splenic or gastrointestinal disease), hypoxia, autonomic nervous system stimulation or with the administration of certain medications.
Runs of >3 repeating VPCs can be classed as an accelerated idioventricular rhythm if the heart rate is less than 160 beats/minute, or ventricular tachycardia if it is above 160 beats/minute.
So how do we manage these?
The first thing we need to do when deciding how to manage anaesthetic arrhythmias is to assess our patient.
What is their pulse rate and how does this compare to their heart rate?
Do they have a pulse for every complex?
How is their pulse quality?
Is their perfusion adequate?
Is their blood pressure normal or is it low?
What is their heart rate, and how often are the abnormal complexes present?
Are they regular and repeating, or intermittent?
Is the arrhythmia progressing?
If the patient has infrequent abnormal complexes, normal blood pressure and good pulse quality, we don’t necessarily need to rush in with medications.
Bradycardic and hypotensive patients with arrhythmias will often require treatment with something like glycopyrrolate.
Tachyarrhythmias such as ventricular tachycardia are generally treated with lidocaine, but intermittent VPCs or AIVR with adequate blood pressure and pulses generally do not require drug treatment.
And one last note on ECGs - though we’re talking about encountering them under anaesthesia, we’ll also see these in many of our medical patients due to their disease process (e.g. splenic masses, hyperkalaemia) - so where this is the case, we need to manage the underlying cause, too.
4: Hypoxaemia
Hypoxaemia is a common complication in anaesthetised patients. We define it as a SpO2 of below 95%. Severe hypoxaemia is defined as a SpO2 below 90%.
Why do we need to use SpO2 to monitor oxygenation? Well, mucous membrane colour isn’t a sensitive indicator of oxygenation - by the time we see cyanosis, the patient will already have significant hypoxaemia (a SpO2 of approximately 80%!).
When do we see hypoxaemia?
Hypoxaemia may occur secondary to:
Hypoventilation (resulting in less oxygen diffusing across the alveolar capillaries into the bloodstream)
One-lung intubation (where an overly long ET tube has been placed, resulting in intubation of a single bronchus rather than the trachea - this means one lung is not ventilating, halving the available space for gaseous exchange)
Atelectasis (where one lung is not inflating due to compression - e.g. in a patient positioned in lateral recumbency for long periods, who is then turned to the other side)
Respiratory disease (e.g. pulmonary diseases reducing the ability for oxygen to diffuse across the alveolar membrane, or pleural space disease reducing the lung’s ability to expand and fill)
Hypoperfusion (where the lungs can deliver oxygen to the bloodstream, but that oxygen is not effectively reaching the body tissues - e.g. due to hypovolaemia)
So how do we troubleshoot a low SpO2?
The temptation when we see a low SpO2 is to think the probe is to blame, reposition it, and see what happens.
And to be fair, the probe usually is the issue - if it’s placed on too small a site, for example, compression will limit blood flow through it, giving us a less accurate reading.
But, before concluding that the probe is to blame, make sure you’ve checked that your patient is intubated appropriately (e.g. the tube is not too far in), still connected to oxygen and that your oxygen is flowing normally, that there are no issues with your circuit, and that complications haven’t been encountered in the procedure itself - such as haemorrhage causing reduced oxygen delivery.
Make sure, too, to think about the patient’s disease process and whether any respiratory compromise is present - and whether this could be causing a drop in SpO2 levels.
Troubleshoot anything you encounter, and then go ahead and reposition your probe, moisten the mucous membranes or tongue, or move the probe to an alternative site altogether.
5: Hypoventilation
Hypoventilation occurs when respiration is insufficient - meaning the body cannot perform adequate gaseous exchange in the lungs.
It can be estimated by observing respiratory rate, depth and pattern; however, this is a very subjective way of assessing ventilation. It is quantified using capnography (giving an ETCO2 reading) or via arterial blood gas analysis (giving a PaCO2 reading).
The normal ETCO2 is approximately 35-45mmHg in conscious patients, and up to 50-55mmHg in patients undergoing surgical anaesthesia. The normal PaCO2 is very similar.
What happens during hypoventilation?
When hypoventilation occurs, hypercapnia results. This accumulation of CO2 leads to respiratory acidosis, and the impaired gaseous exchange leads to hypoxaemia, reducing the amount of oxygen delivered to the cells and tissues.
How do we manage this?
Hypercapnia requires prompt correction when ETCO2 levels exceed 60mmHg. Firstly, assess the anaesthetic depth and reduce volatile agent concentrations as necessary, or give additional analgesia/top-up sedative agents to reduce volatile agent concentrations.
Secondly, check your patient is not inspiring excessive CO2 levels:
Ensure your circuit, adaptors (e.g. HMEs and elbow connectors) and ET tube are not significantly increasing mechanical dead space
Ensure your soda lime is not exhausted if you’re using a rebreathing circuit
Ensure your one-way valves are functioning normally if you’re using a rebreathing circuit
Ensure your flow rate is adequate if you’re using a non-rebreathing circuit
Once you’ve ruled those out, initiate IPPV to reduce CO2 concentrations. In severe ongoing hypercapnia requiring continuous IPPV, the use of a mechanical ventilator is recommended.
Before IPPV or mechanical ventilation, we need to ensure our patient is cardiovascularly stable. This is important as we can reduce venous return, and therefore cardiac output when administering positive pressure ventilation.
So there you have it - 5 of the most common anaesthetic complications we see in our medical patients, and how to troubleshoot them! I hope this has helped you feel more confident monitoring these patients, and given you the tools you need to tackle these common problems.
Which complications do you see most often when monitoring medical patients? Drop me a DM and let me know!
References
American Animal Hospital Association, 2020. AAHA Guidelines > Troubleshooting Anesthetic Complications [Online] AAHA. Available from: https://www.aaha.org/aaha-guidelines/2020-aaha-anesthesia-and-monitoring-guidelines-for-dogs-and-cats/troubleshooting-anesthetic-complications/
