TS/TR Flashcards
1
Q
The tricuspid valve (TV) has a saddle shape because of anterior and posterior high points and mid septal and lateral wall low points.
T or F ?
A
T
2
Q
Tricuspid Valve
The largest leaflet is _________ & the smallest leaflet is ________
A
anterior
posterior
3
Q
Tricuspid Valve
Septal leaflet is connected to the ___________
A
wall of the IVS
4
Q
Tricuspid Valve
How many pap muscles does TV have?
A
3
5
Q
Tricuspid Valve
Compared to MV, TV is positioned slightly ______ than MV
A
inferior
6
Q
Tricuspid Stenosis
Definition
A
TS is a narrowing /thickening/obstruction of the TV that impedes diastolic flow traveling from the RA, though the TV, into the RV
7
Q
Tricuspid Stenosis
Murmur
A
a diastolic rumble that varies with respiration and has an opening snap
*may be accentuated with inspiration
8
Q
Tricuspid Stenosis
cause
A
- RHD: most common cause; however, TS rarely occurs alone, and typically AV and MV are affected prior to TV
- Congenital TS such as Ebstein anomaly
- Carcinoid heart disease with TV involvement: also causes TR, PS, and PR *TV leaflets are thick and rigid with no change in position from diastole to systole
- Secondary TS due to intracardiac wires/pacemaker, RA clot.tumor, or TV vegetation (from endocarditis) that physically obstruct the TV
- Secondary TS due to other medical condition: Systemic Lupus Erythematosus
- Prosthetic valve dysfunction
9
Q
Tricuspid Stenosis
Complications
A
- TS is usually not an isolated disease state and associated with other conditions
- increased risk of infective endocarditis
- increased risk of embolization in the event of a clot or tumor
10
Q
What is Ebstein anomaly?
A
- rare congenital heart defect
- TV is in the wrong position and leaflets are malformed leading to TR
- often associated with ASD and heart rhythm abnormalities
In people with Ebstein anomaly, the leaflets are placed deeper into the right ventricle instead of the normal position. The leaflets are often larger than normal. The defect most often causes the valve to work poorly, and blood may go the wrong way. Instead of flowing out to the lungs, the blood flows back into the right atrium. The backup of blood flow can lead to heart enlargement and fluid buildup in the body. There may also be narrowing of the valve that leads to the lungs (pulmonary valve).
11
Q
Tricuspid Stenosis
signs and symptoms
A
- ascites
- abdominal swelling
- jaundice
- peripheral edema
- right upper quadrant pain
12
Q
Tricuspid Stenosis
Increased RA pressure eventually leads to RA enlargement and signs of _______
A
right heart failure
13
Q
Tricuspid Stenosis
clinical presentation
physical findings
A
- Jagular venous distention with cannon “a” waves
- hepatomegaly
- ascites
- peripheral edema without pulmonary congestion
14
Q
Tricuspid Stenosis
2D echo findings
A
- thickened TV leaflets with restricted motion
- diastolic doming of the TV leaflets best detected from the PLAX or 4C
- decreased TV orifice due to tethered leaflets
- RA enlargement due to volume and pressure overload
- dilated IVC (normal: 1.2-2.1cm) due to the backup of blood and RA enlargement
15
Q
Tricuspid Stenosis
M-mode findings
A
- thickened TV leaflets
- multiple echoes may be visible
- decreased TV leaflet mobility causes a decreased EF slope. The RV fills slower when TS is present; therefore, the valve is help open by an elevated RAP
- anterior motion of the posterior TV leaflet due to tethered TV leaflet tips
16
Q
Tricuspid Stenosis
Quantification
views used to acquire sample volume?
A
- RV inflow
- PSAX
- A4C
- Subcostal SAX
*sample volume at tips of TV leaflets
17
Q
Tricuspid Stenosis
Quantification
Explain how to obtain pressure half time and TVA
A
- Compare PLAX RVIT, PSAX RVIT, A4C, A3C RVIT (modified view), Subcostal 4C/SAX if necessary
- Optimize Doppler angle
- CWD focus within the TV leaflets
- increase sweep speed to 100 mm/s
- Acquire the peak TS waveform, freeze, and measure from the peak velocity down to the deceleration slope *average 3+ waveforms
- The machine will calculate the P½t and TVA once the slope is acquired
18
Q
Tricuspid Stenosis
TVA equation
A
TVA = 190/pressure half time
*190 is constant
19
Q
Tricuspid Stenosis
Similar to MS, TS has an ______ peak velocity (E), _______ EF slope, and _____ A wave that assessed via the pressure half time
A
increased
flattened
absent
20
Q
Tricuspid Stenosis
Explain how to obtain mean PG
A
- Trace the peak waveform, start and finish at ) baseline
- the machine will calculate the mean PG
21
Q
Tricuspid Stenosis
severity scale: TVA
normal?
severe?
A
7-9 cm2
≤ 1.0 cm2
22
Q
Tricuspid Stenosis
severity scale: P½t
severe?
A
≥190 m/s
23
Q
Tricuspid Stenosis
severity scale: mean PG
severe?
A
≥ 5 mmHg
24
Q
Tricuspid Regurgitation
definition
A
the result of an incompetent TV that permits backward systolic from the RV, through the TV (while it is closed), into the RA
25
_Tricuspid Regurgitation_
murmur
a holosystolic murmur that increases with inspiration
26
_Tricuspid Regurgitation_
causes
* majority of normal patients (75%) have trace/mild TR
* mosrt common cause of TR is secondary or functional TR due to:
* annulr dilatation from RA/RV enlargement
* associated with left heart disease
* RV dysfunction
* PH
* myxomatous degeneration - most common cause of primary TR
* Rheumatic TR - usually associated with TS
* TV prolapse \*seen in 20% of cases with concominant MVP (**mid-to-late systolic or holosystolic)**
* incomplete closure of TV due to:
* pacemaker wire
* tumor
* RV infarct
* pap muscle dysfunction
* ruptured TV chordae
* secondary TR due to frail leaflets (closed chest trauma, biopsy, vegetation)
* carcinoid heart disease
* congenital TR (Ebstein anomaly)
* prosthetic valve disease
27
_Tricuspid Stenosis_
severity: inflow time-velocity integral
> 60cm
28
_Tricuspid Stenosis_
severity: supportive findings
enlarged RA ≥ moderate; dilated IVC
29
_Tricuspid Regurgitation_
cause
* **secondary** or **functional TR** due to _annular dilatation_ from RA and/or RV enlargement, may be associated with _left heart disease, RV dysfunction, or PH_ \***most common cause**
* **Myxomatous degeneration** is _the most common cause_ of **primary TR**
* **Rheumatic TR** is usually associated with **Rheumatic TS**
* **TR due to TV prolapse**. **_TVP_** _is seen in_ **_20%_** _of cases with concomitant (associated/accompanied) MVP_ and is diagnosed with excessive billowing of ½/3 TV leaflets into the RA. Similar to MVP, TVP can be mid-to-late systolic or holosystolic
* incomplete closure of TV due to pacemaker wire, tumor, RV infarct, pap muscle dysfunction, ruptured TV chordae
* **Secondary TR due to flail leaflets** (closed chest trauma or biopsy), vegetation etc
* Carcinoid heart disease with TV involvement. TV leaflets are thick and rigid with no change in position from diastole to systole. Additional findings incluude TS, PS, and PR
* Congenital TR such as Ebstein anomaly
* Prosthetic valve dysfunction
30
_Tricuspid Regurgitation_
The majority of normal patients \_\_\_\_% have trace/mild TR (functional TR)
75
31
_Tricuspid Regurgitation_
Functional TR caused by:
* left heart disease (LV dysfunction or valve disease resulting in PH)
* primary PH
* secondary PH due to: chronic lung disease, **pulmonary thromboembolism (DVT)**, left-to-right shunt (ASD/VSD), **AFib**
* cardiac tumors
32
_Tricuspid Regurgitation_
TR due to Structural Abnormality of TV
Cause?
* **25%** of TR patients
* **Rheumatic**
* **Prolapse**
* **Congenital:** Ebstein anomaly, TV displasia, TV hypoplasia, TV cleft, double-orifice TV, _unguarded TV orifice (_most extreme form)
* **Endocarditis**
* **Endomyocardial fibrosis** (an idiopathic disorder of the tropical and subtropical regions of the world that is characterized by the development of restrictive cardiomyopathy and fibrotic changes in the endocardium, usually limited to the cardiac apex.)
* **Carcinoid disease**
* **Traumatic** (blunt chest injury, laceration)
* **iatrogenic**: pacemaker/defibrillator lead interference, RV biopsy, drug exposure to _fenfluramine-phentamine_ (The drug combination fenfluramine/phentermine, usually called **fen-phen**, was an anti-obesity treatment that utilized two anorectics) or methysergide, radiation
33
_Tricuspid Regurgitation_
Backward flow of blood through incompetent TV during ventricular systole. Progressive increase in degree of TR leading to \_\_\_\_\_\_\_\_
RV volume overload
34
_Tricuspid Regurgitation_
Impaired forward cardiac output due to volume of regurgitant flow. Heart compensates for volume overload with ______ and \_\_\_\_\_\_
RV dilatation
hypertrophy
35
_Tricuspid Regurgitation_
Increased RA pressure causes\_\_\_\_\_\_\_ and the process eventually leads to \_\_\_\_\_
RA dilatation
RHF
36
_Tricuspid Regurgitation_
clinical presentation
What are the signs & symptoms?
* usually asymptomatic for a long period
* weakness
* fatigue
* findings of heart failure
37
_Tricuspid Regurgitation_
What are the physical findings?
* Jagular venous distention with prominent “v” wave
* hepatomegaly
* pulsatile liver
* hepatojugular reflux
* peripheral edema
* ascites
* AFib
* hyperdynamic RV impulse
38
_Tricuspid Regurgitation_
treatment options
* TR is usually a secondary problem
* annuloplasty
* valve replacement
39
_Tricuspid Regurgitation_
complications
enlargement of the:
* RA and RV which leads to AFib
* IVC
* hepatic veins
* SVC
* neck veins
40
_Tricuspid Regurgitation_
patient may experience:
* leg and abdominal edema
* liver enlargement
* portal hypertension due to increased BP returning from the venous circulation
41
_Tricuspid Regurgitation_
2D echo findings
\*anatomic basis/defect that prevent coaptation:
* **RA enlargement** with dilated annulus
* thickened TV leaflets, particularly if there is a history of RHD
* **TVP,** best detected from the PLAX RVIT, 4C, or Sub
\***diastolic flutter of the TV leaflets** secondary to trauma or endocarditis
\*_RV volume overload pattern_: **RV dilatation with paradoxical septal motion** - note: chronic, severe TR usually leads to RA/RV dilatation; whereas, normal chamber volume are **_unusua_**l with chronic, severe TR
\*dilated IVC (normal: 1.2 - 2.1 cm)
\*dilated HV (normal: 0.5 - 1.1 cm)
* trauma
* endocarditis
42
_Tricuspid Regurgitation_
Doppler evaluation
hepatic vein evaluation with PWD to check\_\_\_\_\_
hepatic vein flow reversal by aligning insonation beam with the flow in the HV
\*note: may not be reliable in patients with Afib, paced rhythm with retrograded atrial conduction
43
_Tricuspid Regurgitation_
CW Doppler evaluation
What are the disadvantages?
* qualitative
* perfectly central jets may appear denser than eccentric jets of higher severity
* overlap between moderate and severe TR
44
_Tricuspid Regurgitation_
CFD evaluation
* jet size and configuration - jet area to RA area comparison
* direction and eccentricity of jet
* color M-mode to establish timing
\***Vena contracta**
* narrowest portion of jet that occurs at or just downstream from the orifice, measured at the time of its largest diameter
* _not valid_ in presence of multiple jets
* **width \> 0.7** = severe TR
\*PISA
* validated only in small studies
* rarely needed clinically
45
_Tricuspid Regurgitation_
Doppler evaluation
PWD
\*Tricuspid inflow E wave velocity
* predominant early filling with severe TR
* “E” velocity \> 1.0 m/s consistent with severe TR in the absence of severe diastolic dysfunction
* must rule out co-existing stenosis
\*Hepatic vein abnormalities
* Diminished systolic forward flow occurs with increasing severity of TR
* High RA pressure and AFib may also cause diminished systolic forward flow
* severe TR may cause systolic flow reversal
46
_Tricuspid Regurgitation_
TR severity scale
* RVSP/SPAP
* CWD spectral strength and shape
* CFD regurgitant jet area/RA area
* PWD mapping technique
47
_Tricuspid Regurgitation_
CFD severity?
mild
48
_Tricuspid Regurgitation_
CFD severity?
moderate
49
_Tricuspid Regurgitation_
CFD severity?
severe
50
_Tricuspid Regurgitation_
CFD severity?
massive
51
_Tricuspid Regurgitation_
CWD evaluation
Use RV inflow, PSAX, A4C view and evaluate the RA just below the valve leaflets to assess presence of systolic flow disturbance.
T or F ?
T
52
_Tricuspid Regurgitation_
CWD evaluation
Density of CW Doppler signal is proportional to regurgitant volume.
T or F ?
T
53
_Tricuspid Regurgitation_
CWD evaluation
Velocity of TR is NOT related to severity of TR.
T or F ?
T
54
_Tricuspid Regurgitation_
CWD evaluation
Duration of TR signal is typically holosystolic.
T or F ?
T
55
_Tricuspid Regurgitation_
CWD shape of TR
symmetrical shape reflects _____ TR
asymmetrical shape reflects _____ TR
mild
severe \*due to rapid increase in RA pressure
56
_Tricuspid Regurgitation_
CWD evaluation
Use of Bernoulli equation to assess RVSP may be unreliable if the regurgitant orifice is not “restrictive”
T or F ?
T
57
_Tricuspid Regurgitation_
CWD evaluation:
Systolic flow reversal in the _____ vein as viewed in the subcostal LAX of the IVC indicates severe TR
left hepatic
58
_Tricuspid Regurgitation_
CWD evaluation:
CW Doppler from A4C may allow determination of \_\_\_\_\_\_
RVSP (RV systolic pressure)
59
_Tricuspid Regurgitation_
CWD evaluation
RVSP = _____ pressure
systolic PA
\***RVSP = SPAP**
60
_Tricuspid Regurgitation_
CWD evaluation:
RVSP equation?
RVSP = TR jet gradient + RA pressure
61
_Tricuspid Regurgitation_
RVSP/SPAP is dependent upon age, weight, SV, and BP
T or F ?
T
62
_Tricuspid Regurgitation_
In the absence of RVOT obstruction, the peak TR velocity (peak TRV) and mean RAP are used to estimate the RVSP
T or F?
T
63
_Tricuspid Regurgitation_
Even though the sonographer and/or the TR can over/underestimate the values, the RVSP/SPAP has a strong correlation with the noninvasively acquired LAP; therefore, the TR & RVSP/SPAP calculation are used to acquire an indirect estimate of the LAP
T or F?
T
64
_Tricuspid Regurgitation_
The RVSP/SPAP calculation is useful in the diagnosis and assessment of PH
T or F?
T
65
_Tricuspid Regurgitation_
TR & TVSP/SPAP calculation method
1. acquire the **peak TRV** then calculate the **RV-RA pressure gradient** using the modifies Bernoulli equation: **4V2** (\*V = peak TRV you measured)
2. Unless the patient has a _central venous line_, estimate the **mean RAP** by using **3/8/15 method** based on the _IVC diameter & IVC respiratory behavior (collapse)_
* _IVC \< 2.1 cm & collapse_ **_\>_** _50%_ = **normal RAP** = **3mmHg**
* _IVC \< 2.1 cm & collapse_ **_\<_** _50%_ = normal size/**abnorma**l collapse = **intermediate RAP** = **8mmHg**
* _IVC_ **_\>_** _2.1 cm & collapse \> 50%_ = **abnormal** size/normal collapse = **intermediate RAP** = **8mmHg**
* _IVC \> 2.1 cm & collapse \< 50%_ = **abnormal** size/**abnormal** collapse = **severe RAP** = **15 mmHg**
\*acquire _IVC diameter at the end-expiration,_ just proximal to the entrance of hepatic vein
66
_Tricuspid Regurgitation_
RVSP/SPAP equation
RVSP/SPAP = 4V2 + RAP
67
_Tricuspid Regurgitation_
IF the peak TRV = 3.2 m/s, and the IVC diameter = 3.2 cm & collapse \< 50% upon inspiration or sniff test, then what is the RVSP/SPAP?
RVSP/SPAP = 4V2 + RAP
= 4 (3.2)2 + 15
= 56 mmHg
= moderate PH
68
_Tricuspid Regurgitation_
PH severity scale based on RVSP/SPAP:
normal?
moderate?
severe?
normal: 18-25mmHg
moderate: 30-40mmHg
severe: \>70mmHg
69
_Grading the severity of chronic TR by echo_
size of IVC
normal?
normal to mildly dilated?
dilated?
normal: \< 2cm
normal to mildly dilated: 2.1-2.5 cm
dilated: \> 2.5cm
70
What are the reasons that cause a dilated IVC?
* Healthy young athletes may have dilated IVCs in the presence of normal pressures
* The IVC is commonly dilated and may not collapse in patients on ventilators
* In these cases, the IVC size should not be used to estimate RA pressure
71
_Pulmonary Hypertension_
definition
an elevation in the PAP caused by another disease i.e. obstructive sleep apnea, lung disease, diastolic heart failure, left heart disease.
\***It is NOT a disease of the pulmonary vessels themselves**
72
_Pulmonary Hypertension_
PH is identified by:
* elevated SPAP: **\>25mmHg** _at rest_ or **\>30mmHg** _with exercise_
* elevated pulmonary vascular resistance (PVR: the resistance the RV must overcome to pump blood into the PA
73
_PH vs PAH_
What is PAH (pulmonary arterial hypertension)?
a chronic, incurable _subgroup of PH_; it is an _elevation in the PAP_ **caused by pulmonary vessel disease** (the walls of arteries tightens and stiffen)
74
PAH is identified by:
* elevated **SPAP**: \> **25 mmHg** at rest or \> **30 mmHg** with exercise
* pulmonary capillary wedge pressure (**PCWP**) **≤ 15 mmH**g, in other words, a _normal left heart pressure_
* elevated **PVR**
\*According to AHA, patients with PAH with and elevated RAP, pericardial effusion, and moderate to severe TR, have an elevated mortality risk
75
PH associated echo findings:
* abnormal IVS: PWT ratio (\>1)
* diastolic dysfunction (elevated filling pressure by E/e')
* dilated IVC with decreased collapsibility
* dilated PA
* PFO/ASD seen on bubble study
* RVH/LVH, RV/LV dilatation and/or dysfunction
* pericardial effusion
* RAE/LAE
* Significant TR, PR, and/or MR
* ventricular septal flattening; D shaped LV
