TOW open disclosure project (Aus)

principles upon the standards have developed
1) openness and timeliness
2) acknowledgement
3) expression of regret
4) recognition of the reasonable expectations of patients and their nominees
5) staff support
6) integrated risk management and systems improvement
7)good governance
8) confidentiality

aprotinin

A January 26, 2006, article published in the New England Journal of Medicine (NEJM) described the findings from an observational study of 4,374 patients (1,295 treated with Trasylol) scheduled for CABG surgery at multiple centers in multiple countries. 

Compared to those receiving no preventive drug therapy and after propensity adjustment, primary patientsreceiving Trasylol had a higher risk for dialysis or creatinine increase; myocardial infarction or heart failure; or stroke, encephalopathy or coma.  Compared to those receiving no preventive drug therapy and after propensity adjustment, complex patients receiving Trasylol had a higher risk for dialysis or creatinine increase, but not for heart complications, stroke, encephalopathy or coma.  Risks for adverse renal events increased with the administered Trasylol dose.  All three drug therapies (Trasylol, aminocaproic acid or tranexamic acid) were reported to reduce blood loss to similar extents.

risk for death, kidney failure, congestive heart failure and stroke. 

in secondary exposures- risk of anaphylaxis

CPB weaning

 CROSS CLAMP- good visualisation of surgical fields but may result in myocardial ischaemia without adequate protection


 MYOCARDIAL PRESERVATION
crystalloid cardioplegia
Na 147 K 20 Mg 16 Ca 2 Cl 204 procaine 1 mmol/L
cold

does not prevent ion fluxes and continued influx of Ca, Cl , contributing to depletion of ATP and intracellular calcium overload, thought to be critical in development of myocardial stunning

blood cardioplegia
- most common protective strategy
-however- cold blood cardioplegia- increased viscosity- limits myocardial perfusion
-if warm- may reduce reperfusion injury
-improves o2 carriage (compared to crystalloids)
-improves buffering capacity
-multiple doses may be used
-provides antioxidants

for anterograde (via ascending aorta or aortic sinus, with competent AV, Aortic root pressure of at least 60mmHg for coronary perfusion)

alternative cardioplegia methods (without protection)
- intermittent aortic cross clamp/ induced VF

weaning from CPB
- rewarmed to naso/oeso temp 35-36
-core-periph difference <6 degrees)
-shivering-BAD
-overheting-BAD (>36)

intracardiac procedure- de-airing
epicardial pacing wires to protect against arrhythmias
acid base imbalances, electrolytes
ventilation recommenced
anaesthesia/analgesia/nmba suppplemented
monitors
myocardial support instituted

separation
-stable heart rhythm, warm, all above factors addressed
-venous line partially clamped-heart fills
-pump speed reduced-if BP maintains-->
-venous line fully clamped
-pump stopped when heart is appropriately filled and functioning well. (may need tropes, optimal hr)
-can continue to fill with arterial line  


 causes of failure to wean
poor preop ventricular function
inadequate myocardial protection
prolonged cross clamp time
imperfect surgical repair
electrolyte imbalance
acidosis
arrhythmias

TOW the trials

Magpie:

multicentre RCT 10000 women

mag sulph vs placebo

primary outcomes: eclampsia and death of baby

result: 58% lower risk of eclampsia, lower maternal mortality, no diff in baby mortality

TRACman

tracheostomy : early vs late

multicentre prospective RCT

early 1-4, late not before day 10

primary outcome : 30day mortality

CESAR trial:

conventional ventilatory support vs ECMO in severe adult respi failure

mortality and disability lower in ECMO group , likely to be cost effective

VASST trial

vasopressin and septic shock:

low dose 0.01-0.03u/min or norad

NO in ARDS:

no sig diff in groups in mortality, duration, ventilator free days

no group: higher pao2/fio2 on day 1, but increased risk of renal dysfunciton

CTG definitions

ean level of the FHR when this is stable, excluding accelerations and decelerations. It is determined over a time period of 5 or 10 minutes and expressed in bpm. Preterm fetuses tend to have values towards the upper end of this range. A trend to a progressive rise in the baseline is important as well as the absolute values

Normal Baseline FHR
110-160 bpm

Abnormal bradycardia
<100 bpm

Abnormal tachycardia
>180 bpm

Baseline variability
The minor fluctuations in baseline FHR occurring at three to five cycles per minute. It is measured by estimating the difference in beats per minute between the highest peak and lowest trough of fluctuation in a one-minute segment of the trace

Normal baseline variability
Greater or equal to 5 bpm between contractions

Non-reassuring baseline variability
Less than 5 bpm for 40 minutes or more but less than 90 minutes

Abnormal baseline variability
Less than 5 bpm for 90 minutes or more

Accelerations
Transient increases in FHR of 15 bpm or more and lasting 15 seconds or more. The significance of no accelerations on an otherwise normal CTG is unclear

Decelerations
Transient episodes of slowing of FHR below the baseline level of more than 15 bpm and lasting 15 seconds or more

Early decelerations
Uniform, repetitive, periodic slowing of FHR with onset early in the contraction and return to baseline at the end of the contraction

Late decelerations
Uniform, repetitive, periodic slowing of FHR with onset mid to end of the contraction and nadir more than 20 seconds after the peak of the contraction and ending after the contraction. In the presence of a non-accelerative trace with baseline variability < 5 bpm, the definition would include decelerations < 15 bpm

Variable decelerations
Variable, intermittent periodic slowing of FHR with rapid onset and recovery. Time relationships with contraction cycle are variable and they may occur in isolation. Sometimes they resemble other types of deceleration patterns in timing and shape

Atypical variable decelerations
Variable decelerations with any of the following additional components: i. loss of primary or secondary rise in baseline rate, ii. slow return to baseline FHR after the end of the contraction. iii. prolonged secondary rise in baseline rate, iv. biphasic deceleration, v. loss of variability during deceleration, vi. continuation of baseline rate at lower level.

Prolonged deceleration
An abrupt decrease in FHR to levels below the baseline that lasts at least 60-90 seconds. These decelerations become pathological if they cross two contractions, i.e. greater than 3 minutes

Sinusoidal pattern
a regular oscillation of the baseline long-term variability resembling a sine wave. This smooth, undulating pattern, lasting at least 10 minutes, has a relatively fixed

post op visual loss

0.01-1%

commonest causes

- ischaemic optic neuropathy (posterior more common; opthalmic artery branches, risk: hemorrhagic hypotension, not necc with extrinsic compression)

-central retinal arterial occlusion (retinal artery thrombosis: retinal pallor, cherry red spot)

(extrinsic compression)

commonest risk factors:

patient - closed angle glaucoma; male patient, diabetic, hypertension, atherosclerosis, smoking

surgery: prolonged, massive blood loss, anemia

anaesthesia: hypotension, extrinsic pressure on eye, increased CVP (resulting in increased IOP), prone position itself increase IOP (head dependent- worse; head up, better)

ameliorating: position 10' head up, careful no pressure on eye, higher transfusion trigger

myotonic dystrophy

myotonic dystrophy

type 1: congenital/childhood/adult/late

type 2: prox myotonic dys/myo/myopathy syndrome

type 1: unstable trinucleotide expansion

adult onset= autosomal dominant

premature balding, muscle degeneration, cataracts, diabetes mellitus, gonadal atrophy, cardiac abnormalities, adrenal insufficiency, cardiac abnormalities

cardiac- AV delay, atrial tachydysrhythmias, diastolic dysfunction, MVP, cardiomyopathy, sudden death

restrictive lung disease, mild hypoxemia

may have respiratory muscle myotonia-- dyspnea-treat w procainamide

alteration of smooth musc function-gastric atony, intestinal hypomotility

aspiration risk from pharyngeal muscle weakness

pregnancy: may ppt CCF, may need CS for uterine atony

infants of mothers with myotonia-- may develop congenital myotonic dystrophy

Rx: supportive / preventive

sodium channel blockers: less conclusive results

Anaes:

sux : exaggerated contracture-- avoid

chronic myopathy: response to ND NMBA may be exaggerated

muscle stimulation with nerve stimulator: may trigger myotonia

neostigmine: may trigger myotonia

sensitive to respiratory depressant effects

ECT

remote

procedure- pulsed 60 Hz, pulse duration 0.75 ms, total stimulus 1.25s

tonic phase lasting 20s then clonic phase

CVS: parasympathetic stimulation (10-15s) followed by sympathetic : hypertension, dysrhthmias (lasting >=5 min)

CNS: increased CBF, CMRO2, ICP

others: increased IOP and IGP

contraindications- recent AMI, CVA (,3mths) raised ICP, unstable C spine, intracranial mass, aortic aneurysm.

relative:CCF, severe pulm dz, glaucoma, retinal detachment, VTE, thrombophlebitis, angina pectoris

agents : if previous ECTs done, check dosing and adequacy of seizure and adjust accordingly

most preferred=methohexitone (no effect on duration) or propofol (shortens duration of seizure) etomidate: does not shorten seizure duration.

sux 0.5mg/kg or mivacurium 0.08mg/kg

atropine, esmolol drawn up

vacuum insulated evaporator

Oxygen is a non-metallic element existing as a colourless odourless diatomic gas (O2) in the lower atmosphere and as a triatomic oxygen (O3) and monatomic oxygen (O) in the upper atmosphere. Joseph Priestley is usually credited with the discovery of oxygen because he was the first to describe it in 1775 in his work entitled Experiments and Observations on Different Kinds of Air. However Scheele, a Swedish apothecary, first discovered oxygen in 1772. Manufacture of oxygen Oxygen is manufactured by the fractional distillation of air. Air is compressed to 5 atmospheres and cooled to -181oC using reverse heat exchangers. A two-stage distillation process yields 99.5% O2 (and 0.4% argon). It is stored at 137 bar in silver cylinders with green shoulders in the United States. Storage of Oxygen: The VIE Hospitals store large quantities of oxygen as a liquid in a vacuum insulated evaporator (VIE). The inner shell of the VIE is made of stainless steel. It is separated from the outer carbon steel shell by an insulated gap with a vacuum of 0.16-0.3KPa. The contents are at 1000KPa and a temperature of -150oC (critical temp -119oC). A gauge indicates the pressure within and a differential pressure gauge (compares top to bottom) indicates the oxygen contents by weight. Compensatory adjustments made by the VIE system If there is a period of low oxygen use or hot weather this will result in the temperature of the liquid oxygen increasing.. This leads to increased pressure in the VIE and at 1500KPa the blowoff valve opens allowing vaporisation into the environment, (the latent heat of vaporisation cools the liquid oxygen). If there is a period of high oxygen use by the hospital or very cold weather, there will be reflected by a decreased temperature of liquid oxygen and thus a decreased pressure in the VIE system. At 1000KPa the Pressure Raising Valve (PRV) opens, and allows liquid oxygen to shunt through a Pressure Raising Vapouriser (PRV). This allows environmental heat to enter the system. This mechanism ensures that the pressure and temperature of the VIE rises back to normal. All outgoing gases pass through a heat exchanger to warm them.