Cardiac cath diseases Flashcards
SAS
PG is btwn main portion of LV and LVOT
o ↑ systolic peak in body of LV
o PG as KT withdrawn from LV to subvalvular region (95mmHg)
o No systolic gradient at valve level
Valvular AS
PG btwn LVOT and Ao
Supravalvular AS
PG beyond AoV btwn proximal and distal Ao portion
Carbello sign
↑ arterial BP during LV KT pullback with severe SAS
o Related to partial obstruction of already narrowed orifice and subsequent relief when KT is removed
o Seen with patients with AoV area <0.6cm2
Subvalvular PAS
o Pullback 1: systolic P remains unchanged from PA → RVOT
Fall in diastolic pressure indicates entered RV
o Pullback 2: PG with no change in diastolic pressure → intraventricular obstruction
Valvular PS
o Normal PAP and mean RAP
o Abrupt ↑ pressure as KT withdrawn across PV into RV
Systolic PG = 86mmHg
o Slight ↑ a wave secondary to RVH and ↓ RV compliance
Supravalvular PS
o PG is observed when KT is pulled back into MPA
↑systolic pressure with stable diastolic pressure = KT remains in PA, distal to valve
o 2nd pullback: not other systolic gradient → RV
MV stenosis
LAP
o ↑a wave → ↑ residual volume in LA at onset of atrial systole
Can be very large, as high as 50 mmHg
o ↑v wave → ↑LA volume/pressure
Any further ↑ volume in passive atrial filling → increases v wave
o Delayed y descent slope: delayed early/rapid ventricular filling
- PG bwn LA and LV from 5-25mmHg
o ↑LA/PAWP to 20-25mmHg → can lead to
Pulmonary edema
Secondary PH: PVr can ↑ 25-30x normal
o Normal or low LV end diastolic P
o ↓CO secondary to ↓ blood flow across MV
AI
- ↑ LV volume secondary to regurgitation
o ↑SV → ↑ systolic pressure
o Regurgitation during diastole: ↓ diastolic pressure
Diastasis: equalization of diastolic Ao and LVP in severe AI
o Wide pulse pressure - LV workload: progressively ↑ according to magnitude of AI → LV dilation → ↑ wall stress
- Premature MV closure: blood flowing from AI + normal diastole through MV → rapid ↑ LV diastolic P → exceed rapidly LAP → early MV closure
Acute vs chronic AI
o Acute: higher end diastolic LVP → inability to handle ↑ volume
o Chronic: ↑ end diastolic and systolic volume, ↑SV, ↑Ao systolic/mean P + widened pulse pressure
Non restrictive VSD
o ↑RV and PAP equivalent to systemic circulation
o Diastolic/mean PAP remain lower until pulmonary vascular dz develop
o ↑LA/LV end diastolic P → volume overload
MR
- ↑ v wave: reflux of blood in LA during ventricular systole
o Abnormal MV leaflets coaptation
o ↓LA compliance
o Severe MR:
Acute: v wave >2-3x mean LAP/PAWP
Chronic: v wave can be normal as LAE is gradual and can accept enormous MR - Steep y descent: ↑ volume in LA (regurgitant + normal)
- Absent or small a wave
Causes of incr V waves
MR
↑LAP w/o MR
LV failure with large, non compliant LA
Cardiac tamponade
- Equalization of diastolic pressures across all cardiac chambers
o ↑ of diastolic pressures in all chambers - RA waveform:
o ↑a=v waves
o Blunted y descent → ↓ volume from RA/LA to fill RV/LV
o Predominant x descent
o ↑mean RAP = end diastolic PAW/LAP - LV and RV systolic peak pressure out of phase
- Peak AoP varying >10-12mmHg → pulsus paradoxus with respiratory cycles
RCM
- Severe diastolic dysfct with preserved systolic fct
o Diastolic filling restricted by myocardium
o Involves entire myocardium → including IVS
↓ septal shift towards L during inspiration
LVP tracks RVP during systole w respiration (concordant)
o Not associated with ventricular interdependence or intra thoracic/cardiac dissociation - RA waveform: M/W shape
o Rapid x and y descent
o ↑RAP - Ventricular waveform: RV/LV dip and plateau during diastole → rapid early filling with abrupt stop and ↑ end diastolic P
o ↑ diastolic pressures: LV > RV
o Concordant fall in RV and LVP with inspiration - Kussmaul sign → ↑RAP during inspiration