Right heart failure blue book article Flashcards
+Which is the most anterior chamber of the heart?
RV- lies immediately behind the sternum
+How does the RV structure facilitate it’s function?
Thin-walled, low-pressure, maintains pulmonary perfusion pressure & delivers deoxygenated mixed venous blood to pulmonary vasculature for gas exchange, also maintains low systemic venous pressure which prevents organ congestion.
+What shape is the RV in transverse cross-section
crescent
+What’s mean systemic filling pressure (equation)?
MSFP = RAP/(resistance to venous return)
+What’s normal MSFP & RAP & CVP?
MSFP 7-10mmHg
RAP and CVP 0mmHg
+What is the RV blood supply? what does R) dominant circulation mean?
R) CA & it’s branches
in 80% of population the coronary circulation is R) dominant where the R) CA also supplies the inferior wall of the LV & posterior third of the IV septum via the PDA branch. in the other 20%, the PDA arises from the L) CA. So, in 20% of the population, LV perfusion is completely independent of the R) CA.
+How does perfusion of the RV compare with the LV? and the stroke work & O2 demand of the RV?
RV perfusion occurs throughout both diastole & systole due to the lower R) heart chamber pressures. In contrast, LV perfusion occurs primarily in diastole due to higher LV systole & contraction pressures. Due to these lower pressures, the RV has only 25% of the stroke work & lower O2 demand than the LV, despite ejecting the same CO.
+How does the Starling curve of the RV compare to the L)?
It’s flatter, consequently there’s lower variation in RV contractility over a wide range of filling pressures. The RV can tolerate a wider & higher range of preload conditions before it fails.
+What are the pathophysiological mechanisms by which RV dysfunction may occur? How may a more compliant RV cope under these conditions?
Pressure overload (increased afterload), volume overload (increased preload), impaired contractility.
Due to it’s structural characteristics & low muscle mass, a more compliant RV can tolerate increases in preload but is less able to tolerate sudden increases in afterload.
+What are some examples of causes of acute RV failure?
Increased afterload: acute LV failure, APO, ALI, chronic pulmonary HTN, pulmonary infection, pulmonary embolus, chronic lung disease/hypoxia
Impaired contractility/relaxation: myocardial ischaemia/infarction, arrhythmias
other: sepsis, pericardial disease, congenital heart disease, valvulopathies (TCR, pulmonary stenosis), haematological disorders (eg. sickle cell syndrome)
+What are the effects of chronic & acute increased afterload on the RV?
If chronically subjected (eg. chronic pulm HTN), RV progressively hypertrophies & increase contractility to maintain CO.
When compensation mechanisms exhausted, decompensation occurs (eg. RV volume overload–> incr RAP & CVP & systemic congestion–> end organ failure, RV pressure overload dilates the RV, contractility & output reduce, organ failure. May get arrhythmias which reduce coronary perfusion, CO & lead to end-organ failure).
Acute RV afterload increases (eg. acute pulmonary thromboembolism) cause increased RV EDV (dilation & contractility), yet acute compensations are often insufficient to maintain ejection from the thin-walled, less contractile RV & RV dysfunction can rapidly develop. This situation also occurs when an otherwise healthy RV is required to acutely generate mean pressures exceeding 40mmHg.
What are the 3 ways in which a RV chronically subjected to volume overload, which may become dilated & fail, can reduce LV preload?
Reduced RV contractility of the dilated chamber generates insufficient pressure to eject blood through pulmonary circulation
Dilated RV causes an elevated RVEDP which eventually exceeds LVEDP, causing compression/lessening of LV filling & ejection, also the bulging IV septum encroaches on the LV (ventricular interdependence), resulting in relative under filling of the LV
RV tricuspid annular dilatation & TCR reduces forward flow through pulmonary circulation
+How is a dilated RV at more risk of ischaemia?
CorPP= ADP - RVEDP; (same for systole)- so incr RVEDP impedes coronary blood flow.
Dilated or distended RV is predisposed to hypotension-related ischaemia.
Dilated RV also increases R) atrial pressure which impairs systemic venous return, compounding these mechanisms.
+What are examination findings of RV failure? and investigations?
non-specific signs of systemic venous congestion, including:
S3
TCR murmur
elevated JVP
hepatojugular reflux
pulsatile liver
peripheral oedema
and signs of low CO state:
hypotension
tachycardia
cool peripheries
oliguria
Biochemically:
increased lactate
deranged liver biochemistry (liver congestion +/- organ hypoperfusion from inadequate CO)
renal impairment
cardiac biomarkers: BNP, cardiac troponin T non-specific BUT elevations can correlate with reduced RV function after PE if also pulmonary HTN or after congenital cardiac surgery
Early studies: inflammatory biomarkers ST2 & sST2and GT-3 correlate with RV dysfunction in some disease-specific states incl pulm HTN & mechanical support
ECG: may be normal or may show RAD, R) BBB, RVH, S1Q3T3 triad of RV strain may occur
Echo: TAPSE <16mm, FAC <35%, higher MPI (on pulsed doppler >0.43, >0.54 on tissue doppler)
+What proportion of pts with acute pulmonary embolism have the RV strain pattern on ecg of large S wave in lead I, Q wave & inverted T wave in lead III?
up to 10%
+What are strengths of TTE vs TOE for assessment of the RV anatomy & function?
anterior location of the R) heart makes TTE an ideal modality- qualitative assessment methods commonly used to assess RV function have only been validated for TTE.
TOE is limited by distance from the probe to relevant RV structures & poor doppler alignment.
+What are the most-used markers of RV function in TTE?
TAPSE (tricuspid annular plane systolic excursion)- measures movement of tricuspid annular plane longitudinally towards the apex of the RV in systole. Indicates RV free wall longitudinal contraction. Normal >16mm.
fractional area change (FAC)
Myocardial performance (Tei) index
TR (tricuspid regurgitant) jet velocity
+What’s normal TAPSE?
> 16mm
+What’s fractional area change (FAC) & normal value?
A measure of overall RV systolic function, taken in a 4-chamber view, % change in area between systole & diastole.
FAC <35% indicates RV systolic dysfunction.
+What’s the Tei index? in which situations is it not useful? normal values?
myocardial performance index, dimensionless, sum of isovolumetric contraction time & isovolumetric relaxation time divided by ejection time.
useful as it incorporates elements of systole & diastole.
Relies on a constant R-R interval so NOT useful in AF.
Normal values are <0.4 by pulsed doppler & <0.55 by tissue doppler.
+How is tissue doppler imaging used to assess RV function?
measures longitudinal velocity of excursion of regions of the RV during systole- most commonly the tricuspid annulus & the basal free wall segment.
Systolic velocity reported as S’ with <10cm/sec raising suspicion for abnormal RV systolic function.
+What does measurement of the velocity of the TR jet allow?
if a TR jet is present, it permits estimation of RVSP. With the addition of RAP, this measure is equivalent to pulmonary artery systolic pressure in the absence of pulmonary stenosis.
+Pre-operative TTE assessment HAS been shown to predict periop cardiac complications in non-cardiac surgery. Which parameters have predictive value?
lower TAPSE & increased Tei index.
FAC, sPAP & tissue doppler parameters didn’t have predictive value of periop cardiovascular complications.
+What are some conditions that bedside TTE or intraop TOE could identify/exclude in the case of acute deterioration of RV function or unexplained haemodynamic instability?
acute PE
cardiac tamponade
RV MI
acute RV or LV dysfunction
acute valvulopathies
+calculation of EF?
(SV/EDV) x 100
+What’s the most accurate non-invasive technique to assess the RV? parameters?
cardiac MRI
mass, volume, EF, scar burden, myocardial strain, perfusion
