Venous gas embolism blue book article and *hyperbaric medicine blue book article Flashcards
Why is the presentation of VGE so variable, from asymptomatic to cardiac arrest to catastrophic brain injury or death?
absolute quantity of gas varies
type of gas (most commonly air) varies
end location may be venous, pulmonary or arterial
the area impacted may have varying collateral circulation
metabolic requirements & susceptibility to vascular inflammatory changes vary
How may venous gas embolism subsequently arterialise (paradoxical embolisation)?
via intra-cardiac (PFO, ASD) or intra-pulmonary (overwhelming the filtration capability of pulmonary capillaries or via intrapulm A-V anastomoses) shunting
What types of procedures may risk direct arterial gas embolism?
cerebral angiography
open chamber cardiac surgery
bypass circuit accidents
extremely rarely via atrial-oesophageal fistulae
What are the preconditions for entry of gas into the venous system? And what are other causes of venous gas embolism related to surgical procedures?
opening of non-collapsing veins to atmosphere
sub-atmospheric pressure within the vessels
situations where the surgical site is under pressure
surgical wound situated above the level of the heart, enabling passive air entry (eg. shoulder)
veins within a coagulated operative field may allow entry of air
air may enter through CVC or haemodialysis catheters, mainly on insertion removal but potentially due to detachments/breaks in the lines
myometrial veins during pregnancy & after delivery are particularly susceptible to air entrainment.
Examples of non-collapsing veins?
epiploic
emissary
dural venous sinuses
At what flow rates are the majority of bubbles able to be filtered by pulmonary capillaries?
up to 10mL/min
What’s the sequence of events with a rapid or large volume of air entrained into venous circulation?
raised pulmonary artery pressure
increased RV preload
acute RV failure & reduced output
impaired pulmonary venous return/LV preload/CO & organ perfusion; cardiovascular collapse; tachy or bradyarrhythmias may develop
Due to the altered pulmonary resistance, R) -> L) intrapulmonary shunting & incr alveolar dead space ventilation, V/Q mismatch & hypoxaemia ensue
How may cerebral arterial gas embolism (CAGE) occur?
direct injection of gas into cerebral arterial system during angiography or paradoxical embolism via intracardiac, intrapulmonary or other shunting.
pulmonary barotrauma can enable entry of gas into pulmonary veins, L) hear & subsequently cerebral circulation.
Why & how is CAGE a biphasic phenomenon?
initial temporary neurologic dysfunction due to transient lodgement of bubbles in the cerebral circulation
most are cleared into the jugular veins (relatively high cerebral arterial systolic pressure, almost two-fold greater diameter of the venous end of a cerebral capillary cf the arterial end (bubbles sucked through capillaries into the veins))
Then, 65% get a secondary deterioration which may be several hrs later, due to interaction btwn gas bubbles & vessel walls (eg. endothelial damage, activation of clotting cascade)–> vascular inflammation, secondary thrombotic occlusions & oedema, secondary vasospasm.
What happens if bubbles are distributed to brainstem?
cardiorespiratory arrest
frequently fatal
What are some of the signs of cerebral gas embolism? and pulmonary?
Usually rapid onset: confusion, stupor, headache, vertigo, dizziness, focal neurological deficits (motor, sensory, speech, visual field defects mimicking stroke), gait disturbance, loss of consciousness.
Chest pain, shortness of breath, cardiac arrest.
In which situations (which make up approximately 30% of cases of arterial gas embolism) is ischaemia, infarction & symptoms consistent with a stroke syndrome more likely to occur?
larger intra-arterial cerebral bubbles particularly within loop and anastomotic vessels which are subject to systolic pressure @ both ends or bubbles occupying many generations of arterioles
How to prevent & diagnose vascular gas embolism?
Clinical diagnosis
High index of suspicion & attention to physiologic variables during procedures for which vascular embolism is a known risk
Consider surgical position, consider pre-op workup (eg. TTE or TOE to exclude PFO before seated craniotomy)
DISCUSS RISK PRIOR TO PROCEDURE & DURING TIME-OUT
Aim to maintain preload (minimise air entrainment)
Care re: pt positioning & monitoring (eg. lower threshold for art line)- head-down for CVCs, minimise time with open connections, pt should breathe all the way out when insert
Be attentive to the sound of sucking in of air or visible entrainment through lines or cannulae
Be vigilant particularly at key risk points of the procedure- maintain excellent communication with surgeon- culture of “speaking up” fostered, consider vascular gas embolism among interdepartmental SIM training
Look out for sudden:
hypoT (accumulating RV air–> RVOTO, acute RV failure which compromises LV output & –> CV collapse
tachycardia or bradycardia
arrhythmias or ischaemic changes on ecg (eg. air entrained into coronary circulation esp LAD)
cardiovascular collapse
pulmonary oedema or acute lung injury due to inflammatory cascade
reduced EtCO2 (due to headspace ventilation)- may detect 0.5mL/kg venous air
decreased SpO2
hypoxaemia & hypercarbia on the ABG depending on degree of V/Q mismatch
sudden sustained fall in BIS or cerebral oximetry
seizure activity
transient or persistent ST changes
“mill-wheel” splashing murmur of froth in cardiac chambers & great vessels
may have failure to wake from GA (arterial air embolism may –> ischaemic stroke)
an awake pt: confusion, headache, stroke signs, chest pain/palpitations (may see arrhythmias or ischaemia on ecg), may pleural substernal-chest pain, tachypnoea, dyspnoea, cough, PAE typically causes signs of angina or embolic stroke. late sign= haemoptysis. abdo pain, bowel iscahemia.
May develop SIRS type syndrome & multi organ failure
do not be falsely reassured by resolution of S&S (injury may be biphasic)
are cardiopulmonary symptoms (eg, tachypnoea, hypocapnia, pulmonary oedema, cardiac arrest) more common with venous or arterial air embolism?
venous
How does symptom onset & type vary with arterial vs venous?
immediate onset if gas injected directly into arterial system- more often confusion, LOC, focal neurological deficits, cardiac arrhythmias or ischaemia.
venous air arterialising is a slower process; symptoms rely on increase in pulm artery pressures & incr R) heart pressures
What’s the gold-standard for detection of air embolism? is there a threshold of intra-vascular air which is significant?
TOE (can detect as little as 0.02mL/kg of air)
no threshold since the outcome of vascular gas embolism depends on the vessels lodged into & other factors
What’s the role of cerebral radiological imaging for CAGE?
only to exclude other causes that might present like AGE (eg. intracerebral haemorrhage)
high false -ve rate for CAGE even if severe neurological deficits, imaging should NOT be relied on for diagnosis
in cases highly suggestive of CAGE (eg. high-risk procedure), imaging is not recommended as it delays time to definitive Rx (recompression)
Management for iatrogenic vascular gas embolism?
- PROMPT RECOGNITION:
- Call for help, communicate the emergency & delegate - MINIMISE FURTHER AIR ENTRAINMENT:
Prevent further entrainment of gas by:
- flooding the field with irrigation fluid
- temporarily occluding the vessel
- ceasing insufflation
- decompressing any pressurised systems
- position operative site below heart
- stopping any procedures through which air may be entrained (eg. reaming of bones during ortho surgery)
- SUPPORT AFFECTED ORGAN SYSTEMS
- Secure airway if not already in place, ventilate w 100% O2 to maintain arterial oxygenation & facilitate de-nitrogenation & resorption of bubbles. Avoid N2O.
- maintain normovolaemia to optimise microcirciulation
- use Adr/other vasopressors/inotropes for haemodynamic support
- place L) lateral position if unconscious, trendelenburg no longer routinely recommended (risk worsening cerebral oedema, doesn’t keep bubbles from being distributed to systemic circulation)
- supine if awake or protected airway BUT if RVOTO by gas embolism, immediate placement into L) lateral decubitus & trendelenburg may relieve air lock & move air into RA
- if arrest, likely PEA or asystole
- AIM TO HALT THE PROGRESS OF ALREADY ENTRAINED AIR
- COULD CONSIDER aspirating CVC if in situ (emergent placement for this purpose isn’t evidence-based) & for venous gas embolism closed cardiac massage to break up large volumes of air in the cardiac chambers, forcing air into smaller vessels, improving blood flow. - DEFINITIVE Mx= HYPERBARIC O2:
- after successful resus, consider hyperbaric O2 therapy & ICU
Is trendelenburg routinely recommended? why? what positions recommended in certain circumstances?
No. theories about mechanisms not experimentally confirmed, trendelenburg risks worsening cerebral oedema (a big risk given that large air emboli increase ICP from 12-52mmHg within 2 hrs of insult)
HOWEVER, if sudden RVOTO by gas embolism, immediate placement into L) lat decubitus & trendelenburg may relieve air-lock & move air into RA.
If the pt awake with protected airway, place supine
if unconscious with unsecured airway, lateral decubitus
What’s the only definitive Rx for arterial gas embolism?
Hyperbaric oxygen treatment. There’s an AHA class 1 recommendation (level C evidence) for this indication
many studies show improved neurological outcomes, neurophysiological studies & neuro-psychometric testing among pts with arterial gas embolism treated with hyperbaric O2
How soon after an air embolism event should hyperbaric oxygen be delivered? Is it, however, recommended for isolated venous gas embolisation?
ASAP- better neurological outcome if within 8 hrs of CAGE. Even if pt appears to have spontaneously recovered, early HBOT still recommended given can be biphasic, later benefits may occur with modulation of post-bubble vascular inflammatory changes.
Evidence for HBOT in isolated venous gas embolism is less clear; not recommended for asymptomatic venous gas embolism.
How does HBOT work?
reduces gas bubble volume by increasing ambient pressure (Boyle’s law; P1V1=P2V2)
this allows the bubbles to be resolves or redistributed, restoring blood flow.
As per Henry’s law (C = kP), HBOT increases the solubility of the culprit gas, enabling resorption & increasing the amount of dissolved oxygen, improving tissue oxygenation.
Hyperoxia creates a diffusion gradient of O2 into gas bubble & N2 out (it eliminates inspired O2). Rate of bubble resolving depends on the diffusion of nitrogen out of the bubble & transport of dissolved gases to lungs.
HBOT also reduces leucocyte adhesion to damaged endothelium, reduces inflammation & limits ischaemia-reperfusion injury.
What’s the dose for hyperbaric treatment of air embolism? why this dose? How many treatments?
compression with 282kPa, breathing 100% O2
this dose causes rapid bubble volume reduction, acceptable risk O2 toxicity & is safe for nurse attendant wrt nitrogen narcosis & decompression illness
short & cheap Rx
generally 1-3 treatments until response plateau reached & maintained
What’s the recommendation for lignocaine in AGE? What dose use? possible mechanisms?
Class IIa AHA recommendation, level B evidence
Good evidence in animal studies.
If used, aim for a serum lignocaine [] of 2-6microg/mL, consistent with an anti arrhythmic effect
cerebral neuro protection, reduces leucocyte migration, modulates haemodynamic parameters
