2018 Feb FRCA Flashcards
1.1 Define Sedation
Sedation, also known as “monitored anesthesia care”,
is a continuum
ranging from minimally impaired conciouesness to unconciousness
Medications are given,
usually through an IV,
to make the patient feel drowsy and relaxed.
Different levels of sedation are possible, depending on the type of procedure and the patient’s preference.
1.2 What are the ASA Classifications of Sedation?
- Minimal Sedation
Anxiolysis - Moderate Sedation/Analgesia
(“Conscious Sedation”) - Deep Sedation/
Analgesia - General Anesthesia
What are the clinical criteria at each level?
- Responsiveness
- Airway
- Spontaneous Ventilation
- Cardiovascular Function
Responsiveness
- Normal response to verbal stimulation
- Purposeful** response
to verbal or tactile
stimulation - Purposeful** response
following repeated
or painful stimulation - Unarousable even
with painful stimulus
Airway
Unaffected
No intervention required
Intervention may be required
Intervention often require
Spontaneous Ventilation
Unaffected
Adequate
May be inadequate
Frequently inadequate
Cardiovascular
Function
Unaffected
Usually maintained
Usually maintained
May be impaired
1.4 Dissociative Sedation
Trancelike
cataleptic state
profound analgesia and amnesia
Maintaining protective airway reflex
spontaneous resp
CV stability
Between moderate and deep
1.5.a
What is the mechanism of action of midazolam?
Midazolam is a γ-aminobutyric acid A (GABAA) receptor agonist
This results in the sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties for which the drugs are prescribed.
1.5.b What is it’s time to peak onset
and elimination half life
IV Onset ~2 min
Maximum effect is in about 5 to 10 minutes.
The elimination half-life of midazolam is between 1.5 - 2.5 hours
What adverse errors can occur with sedation and causes of same
Dose
Inappropriate dose given - causing over sedation
Respiratory compromise
Certain agents - ie midazolam can affect respiratory effort - in extreme may require advanced resp support
HD compromise
Propofol can lead to decrease in CO / drop in SVR - may cause hypotension
Aspiration
Deeply sedated patient may lose protective airway reflexes and are at risk of aspiration of gastric contents
Delirium
Increased risk of delirium in older age group
Agitation / hyperactivity
Midazolam can cause a paradoxical hyperactivity in some patients
2.1 Define counter -pulsation
Counter-pulsation is a term that describes
balloon inflation in diastole
and deflation in early systole.
2.2 Physiological mechanism of IABPs
Inflation: >> Forces blood proximally, increasing the pressure within the proximal aorta compared to the left ventricle, thus improving perfusion of coronary arteries, increasing oxygen delivery.
> > Forces blood distally,
thus augmenting the apparent
output from the left ventricle.
> > Augments Windkessel effect.
Deflation:
» Decrease in afterload reduces myocardial wall stress during systole, thus
reducing myocardial oxygen demand.
2.3 Indications for IABP
Indications:
» Cardiogenic shock due to myocardial infarction if revascularisation planned.
> > Acute mitral regurgitation or ventricular septal defect due to acute myocardial infarction.
> > Refractory ventricular arrhythmias whilst awaiting definitive treatment.
> > Refractory unstable angina if treatment option available.
> > Refractory left ventricular failure if destination treatment planned.
> > Perioperative support for high-risk coronary artery bypass surgery.
> > Perioperative support for high-risk non-cardiac surgery
2.3 ContraIndications IABP
Contraindications:
Absolute
» Aortic regurgitation, dissection or stent.
> > Chronic end-stage heart disease with no further possible intervention.
Relative
> > Uncontrolled sepsis.
> > Abdominal aortic aneurysm, severe peripheral vascular disease or arterial reconstruction surgery.
> > Uncontrolled bleeding disorder.
> > Tachyarrhythmias.
2.4 List the possible complications
of an IABP. (6 marks)
> > Haemodynamic compromise due to poor timing of counter pulsation or malposition.
> > Limb, spinal cord or visceral (especially renal) ischaemia.
> > Compartment syndrome.
> > Aortic dissection.
> > Vascular injury causing bleeding, haematoma, false
aneurysm, arteriovenous fistula.
> > Cardiac tamponade.
> > Thromboembolism.
> > Thrombocytopaenia and haemolysis.
> > Infection.
> > Balloon rupture resulting in gas embolus.
3.1 Abdominal Compartment Syndrome
Define Intra Abdominal Hypertension
Intra-abdominal hypertension is a sustained or repeated IAP > than 12 mmHg
Define Abdominal Compartment Syndrome
Abdominal compartment syndrome is defined
as a sustained IAP greater than 20 mmHg
with a new organ dysfunction or
failure regardless of
abdominal perfusion pressure (APP)
3.3 Systemic effects of Abdominal Compartment Syndrome
CVS
Resp
Systemic effects of intra-abdominal hypertension
Cardiovascular effects of increased intra-abdominal pressure
1 Reduced venous return
2 Reduced cardiac output
3 Increased systemic vascular resistance
Pulmonary effects of increased intra-abdominal pressure:
1 Reduced PaO2/FiO2 ratio
2 Hypercarbia
3 Increased inspiratory pressure
3.3 Systemic effects of Abdominal Compartment Syndrome
Renal
CNS
GI
Renal effects of increased intra-abdominal pressure
1 Reduced glomerular filtration
2 Oliguria
CNS
Acute elevations of IAP may also increase intracranial pressure.
Gastrointestinal effects
Gut mucosal ischaemia, independent of changes in cardiac output,
occurs with an increase in IAP
3.3 - Pathphpysiology of AC
Pathophysiology
Chronic increase in intra-abdominal volume
can be compensated by changes
in the abdominal wall compliance.
In situations where the volume of the
abdominal contents increases rapidly or the
abdominal wall compliance reduces,
IAP increases.
Initially, the abdominal wall distends but, eventually,
a critical volume is reached and the compartment syndrome occurs.
Factors such as the rapidity of the increase and the presence of muscle spasm secondary to peritonism can affect the critical volume.
A rapid increase in the volume of the
abdominal contents occurs in many situations such
as haemorrhage or blunt abdominal trauma.
Also, capillary leak, interstitial oedema and disseminated intravascular coagulation may result in ascites, ileus and bowel wall oedema.
Gas, whether inside or outside the bowel, faeces and foreign bodies, e.g
. surgical packs, can all contribute to the
increase in pressure.
3.4
Anaesthetic considerations for patient coming to theatre for treatment of
Abdominal Compartment Syndrome
Anaesthetic management for abdominal decompression
1 Severe instability may preclude the transport of the patient to the operating theatre.
2 Although concerns have been raised about the potential difficulty of managing haemorrhagic complications,
many centres now routinely perform decompression within the Intensive Care Unit.
3 The pharmacokinetics and pharmacodynamics of anaesthetic agents may be altered in the presence of intra-abdominal hypertension.
4 Patients with ACS may be more sensitive to the cardio- vascular depressant effects of anaesthetic agents; changes in organ blood flow and altered volumes of distribution may increase their potency
3.4 Anaesthetic considerations for patient coming to theatre for treatment of
Abdominal Compartment Syndrome
The abdominal decompression syndrome
During abdominal decompression, three potentially dangerous physiological changes occur.
- A sudden drop in systemic vascular resistance
Although the use of epinephrine has been advocated inthis situation, most centres use an approach of aggressive preloading with fluids.
- A fall in intrathoracic pressure Many patients with ACS require ventilatory pressures of
approximately 50 cm H 2 O together with high levels of
PEEP.
Sudden decreases in intrathoracic pressure may
result in the administration of inappropriately large tidal
volumes and alveolar over-distension, producing both
barotrauma and volutrauma.
3 The washout of toxic products
Ischaemic metabolism causes accumulation of lactic acid, adenosine and potassium within the tissues. Following the restoration of circulation, these products rapidly return to the general circulation producing arrhythmia, myocardial depression and vasodilatation.
Asystolic cardiac arrest has been reported in up to 25% of patients undergoing decompressive laparotomy and is reported as being universally fatal.
The decompression syndrome may be ameliorated by the prior administration of a ‘reperfusion cocktail’.
This consists of 2l of 0.45% normal saline containing 50 g of mannitol and 50 milliequivalents of sodium bicarbonate.
3.4 Anaesthetic considerations for patient coming to theatre for treatment of
Abdominal Compartment Syndrome
Management after decompression
Closure of abdomen after decompression may not be possible for several days because of bowel oedema.
Fluid requirements in a patient with an open abdomen are massively increased (up to 10–20 l day1 ).
Hypothermia remains a risk and core temperature monitoring is required.
Despite decompression, ACS may recur.
Therefore, intravesical pressure monitoring should continue after decompression.
Enteral feeding is well tolerated by patients with an open abdomen and may speed the resolution of gut oedema.
Reperfusion injury to the gut and kidneys may also occur after delayed decompression with subsequent development of multi-organ dysfunction