Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Fellowship revision > Management of RV dysfunction after separation from CPB blue book article > Flashcards

Management of RV dysfunction after separation from CPB blue book article Flashcards

1
Q

What is the precipitous spiral that can occur with RV failure?

A

RV failure
hypotension
further RV dysfunction
poor LV function & decreased systemic arterial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which heart chamber can better tolerate sudden changes in afterload?

A

muscular LV

When faced with high afterload, the RV dilates, reducing it’s contractility & SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which heart chamber better tolerates moderate increases in preload?

A

RV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does ventricular interdependence refer to?

A

how the size, shape & compliance of one ventricle affects the haemodynamic properties of the other. Main determinants= the inter ventricular septum (systolic interdependence), pericardium (diastolic interdependence) , shared blood supply & continuity of the myocardial fibres btwn RV & LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does ventricular interdependence refer to?

A

how the size, shape & compliance of one ventricle affects the haemodynamic properties of the other. Main determinants= the inter ventricular septum (systolic interdependence), pericardium (diastolic interdependence) , shared blood supply & continuity of the myocardial fibres btwn RV & LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

At greater than what RA pressure is RV dysfunction likely to be present?

A

8-10mmHg
or if RA:PCWP index is >=0.8 (higher= associated with higher PVR & reduced RV function) & the patient has a cardiac index of <2.2L/min/m2
These measures are in spont vent, non-sedated adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What measures raise suspicion of RVOTO?

A

RV to pulmonary artery pressure gradient of >25mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What measures raise suspicion of RVOTO?

A

RV to pulmonary artery pressure gradient of >25mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What’s cardiac index?

A

relates the CO from the LV in 1 minute to BSA, normal 2.5-4L/min/m2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the risk factors for developing post-CPB RV failure?

A

pre-existing RV dysfunction
pulmonary HTN
long CPB times
LVAD insertion (RV failure post LVAD insertion occurs in 20-40% of cases)
heart transplantation (particularly if the donor heart had a long ischaemic time or if mismatched in size)
inadequate myocardial protection (provided while on CPB with cardioplaegia, flooding the surgical field with CO2)
protamine (pulmonary HTN increasing RV afterload is a known side effect)
any obstruction to R) coronary blood flow- a common etiology= inadequate de-airing of the LV prior to coming off CPB. Other aetiologies of decreased flow through R) CA include failed grafting, suturing, occlusion of coronary Ostia during valve surgery, acute thrombus at Ostia or RCA lumen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Strategies to limit the risk of RV dysfunction

A

optimise ABG (avoid acidaemia, hypoxaemia & hypercapnia) & ventilatory (avoid excess TVs & PEEP) settings to avoid pulm VC

delivery of pulmonary vasodilators, which may be commenced pre-bypass in susceptible pts (eg, those with pre-existing RV dysfunction, pulm HTN, LVAD or heart transplant). Eg. NO, via insp limb of anaesthetic circuit from specific NO delivery system, concentrations monitored & controlled in ppm (starting at 10-20ppm, increasing to 40ppm as desired).
Other options= inhaled milrinone, inhaled prostacyclin such as epoprostenol & iloprost.

aggressive de-airing prior to weaning off CPB.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What’s an advantage over inhaled iloprost vs milrinone and epoprostenol?

A

iloprost is easier to administer. Doesn’t need to be a continuous infusion (unlike NO & epoprostenol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What’s a problem with epoprostenol? how to overcome

A

may cause bleeding due to anti platelet activity

this complication is seen less with inhaled vs IV epoprostenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is CO2 embolism less significant than air?

A

dissolves more rapidly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Does ejection fraction form part of the routine TOE examination of the RV?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the recommended ASE assessment of RV function?

A

RV size (volumetric quantification is challenging, visual estimation is common)
RA size
systolic PA pressure (estimate RA pressure using IVC dimensions)
a measure of RV systolic function, either FAC, TAPSE, tricuspid annulus peak velocity +/- RV index of myocardial performance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How many mid-oesophageal views are there?

A

15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How many mid-oesophageal views are there?

A

15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How many transgastric views are there on TOE?

A

9 (looking through diaphragm to heart)

17
Q

How many aortic views are there on TOE?

A

4

18
Q

What does the mid-oesophageal view of the RA allow?

A

interrogation through the TCV to the RV apex, allowing assessment of the apical portion of the anterior RV free wall

19
Q

What does the deep transgastric view of the RA allow?

A

representation of the RV inferior wall, with ante flexion of the probe can view the RV inflow tract & pulmonary valve

20
Q

How is the RA best visualised on echo?

A

mid-oesophageal 4-chamber view, mid-oesophageal RV inflow/outflow view & bicaval view

21
Q

How are the pulmonary valve & arteries best viewed on TOE? how to assess flow characteristics?

A

mid oesophageal RV inflow-outflow view (pulmonary valve) & upper oesophageal views (pulmonary arteries)
doppler

22
Q

Given that a comprehensive RV TOE assessment is not feasible when weaning from CPB, a focused exam should be performed comprising of what?

A

assess RV free wall, septal wall, RV inflow tract, RV outflow tract, TAPSE

23
Q

what’s an abnormally thick RV free wall?

A

> 0.5cm

24
Q

What’s abnormal RVEF?

A

<45%

25
Q

what’s abnormal pulsed doppler peak tricuspid annulus velocity?

A

<9.5cm/s

26
Q

What represents high RA pressure?

A

> 5mmHg

27
Q

What represents high tricuspid regurgitation velocity?

A

> 2.8m/s

28
Q

What represents high systolic pulmonary artery pressure?

A

> 35mmHg

29
Q

While there’s no agreed perfect index of RV function, what are the most useful views to rapidly assess RV dysfunction? other TOE features indicating RV failure?

A

mid-oesophageal 4-chamber view
RV inflow-outflow view to analyse TAPSE
placing colour flow doppler across tricuspid valve to assess for new/worsening TCR

Evidence of increased RA pressure (eg. bowing of inter-atrial septum, dilated IVC with reduced collapsibility)
incr RV to LV size ratio >0.6
flattened or L)-deviation of IV septum (usually convex to RV)

30
Q

How may cardiac surgery confound measures of TAPSE & tricuspid annulus peak velocity (S’)?

A

CPB & chest closure decrease these measurements

31
Q

What are some CVP parameters that may indicate failing RV?

A

CVP (surrogate for RA pressure) >20mmHg
CVP > PCWP
cardiac index <2.1L/min/m2
fusion of c & v waves implies new TCR & failing RV

31
Q

What are some CVP parameters that may indicate failing RV?

A

CVP (surrogate for RA pressure) >20mmHg
CVP > PCWP
cardiac index <2.1L/min/m2
fusion of c & v waves implies new TCR & failing RV

32
Q

What’s the diastolic slope of the RV pressure waveform in a normal RV? what happens as RV dysfunction occurs?

A

almost horizontal
begins to upslope
as RV function deteriorates further, it takes a square root shape
finally there’s equalisation of the RV & PA diastolic pressures
with severe RV failure, there’s delay in systolic upstroke & RV pulse pressure reduces

33
Q

What’s the pulmonary artery pulsatility index (PAPi)?

A

a new measure in assessment of RV dysfunction, particularly post RV infarction, advanced HF, cariogenic shock & LVAD implantation

PAPi = (systolic PAP - diastolic PAP) / RAP

thresholds not established

34
Q

How should management of RV preload be managed when coming off CPB?

A

If the RV has normal afterload, fluid loading will assist in maintaining SV. If R)-sided filling pressures are low (CVP <15mmHg & RV is not dilated on TOE), judiciously volume load.
If RV has high afterload, fluid loading will cause L)-shift of the RV, ventricular interdependence comes into play & reduced LV filling & SV ensues. If RV preload is elevated, reduce by encouraging venous pooling; raise head of table or start GTN infusion to dilate capacitance vessels. could reduce preload by asking perfusionist to empty blood into the bypass circuit via aortic cannula.
maintain sinus & treat any high-degree AV block; pacing useful to reduce worsening haemodynamic function.
If the RV is hypertrophied & non-compliant in the setting of pulm HTN, it relies on the atrial kick- atrial epicardial leads could be placed.
prioritise conversion to sinus with electrical or chemical means (supraventricular arrhythmias poorly tolerated)

35
Q

what are causes of high afterload coming off bypass? how to mitigate risks?

A 
atelectasis
academia
reperfusion injury
endothelial damage & release of inflammatory mediators
hypoxia, hypercapnia
hypothermia

ABG, ensure no acidosis
PiO2 100%
set ventilator to avoid hypercarbia or excess TVs & PEEP (gentle ventilatory recruitment to promote parenchymal lung blood vessel opening)
warm

consider inhaled pulmonary VDs once ventilatory & physiological parameters addressed (NO, prostacyclin, iloprost, milrinone)

36
Q

Advantages of inhaled vs systemic pulm vasodilators?

A

reduce PVR with less systemic hypoT & V/Q mismatch

37
Q

How increase RV contractility coming off bypass? side benefit? other option?

A

dobutamine: increases RV contractility & lowers PVR
milrinone is an alternative but may produce more profound systemic hypoT vs dobutamine which risks impaired coronary perfusion & spiral of RV dysfunction
May offset hypotension with these inotropes with vasopressor (NAdr low-dose or vasopressin)

38
Q

What’s 1st line for sudden post-CPB severe RV failure?

A

adrenaline. significantly improves RV EF.

other option for post-CPB RV failure is intratracheal milrinone 5mg- efficacy of 60% in restoring RV function.

39
Q

Best drug to use for the vital role of maintaining systemic BP to sustain R) coronary perfusion?

A

vasopressin: minimal effects on PVR but increases SVR

40
Q

Best drug to use for the vital role of maintaining systemic BP to sustain R) coronary perfusion?

A

vasopressin: minimal effects on PVR but increases SVR

41
Q

Order of management for RV failure coming off CPB?

A

assess RV preload. If CVP <15mmHg & RV not dilated on echo, give small fluid challenge (eg. pump blood)
if preload high, lower by head up or removing blood from circulation in to CPB circuit, commence GTN if these measures inadequate
concurrently, have a vasopressor (ideally vasopressin) running to support coronary perfusion
increase RV contractility with dobutamine, consider adrenaline or milrinone
if haemodynamic compromise, consider add small boluses or intratracheal 5mg milrinone
maintain SR & AV synchrony (cardioversion chemically or electrically, AV pacing
consider inhaled pulm VD for raised PA pressures or IV
unresponsive cases with severe haemodynamic instability, consider a return to CPB (which may incr M&M), IABP to promote RCA flow or V-A ECMO or RVAD can be considered.

Fellowship revision (78 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions