Cardiac cath diseases Flashcards

1
Q

SAS

A

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o PG as KT withdrawn from LV to subvalvular region (95mmHg)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

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2
Q

Valvular AS

A

PG btwn LVOT and Ao

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3
Q

Supravalvular AS

A

PG beyond AoV btwn proximal and distal Ao portion

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4
Q

Carbello sign

A

↑ 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

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5
Q

Subvalvular PAS

A

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

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6
Q

Valvular PS

A

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o Abrupt ↑ pressure as KT withdrawn across PV into RV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

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7
Q

Supravalvular PS

A

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

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8
Q

MV stenosis

A

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
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9
Q

AI

A
  • ↑ 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
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10
Q

Acute vs chronic AI

A

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

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11
Q

Non restrictive VSD

A

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

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12
Q

MR

A
  • ↑ 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
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13
Q

Causes of incr V waves

A

MR
 ↑LAP w/o MR
 LV failure with large, non compliant LA

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14
Q

Cardiac tamponade

A
  • 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
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15
Q

RCM

A
  • 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
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16
Q

Constrictive pericarditis

A
  • Ventricular interdependence: filling of 1 ventricle impairs filling of the other (mechanical constraint of pericardium)
    o Discordant changes in R/LV systolic pressures during inspiration
    o Respiratory fluctuations:
     Inspiration: ↓ intrathoracic pressures NOT communicated to heart chambers
  • No respiratory changes in RAP
  • Kussmaul sign: ↑RAP in severe cases
  • Ventricular waveform:
    o RV/LV dip and plateau during diastole → rapid early filling with abrupt stop secondary to volume limit from stiff pericardium
    o ↑ end diastolic P: LV = RV
  • RA waveform: M/W shape
    o ↑/rapid y descent → rapid filling in early diastole
    o Steep A wave
    o Blunted x decsent → atrium attempt to fill an overfilled/full ventricle
17
Q

Double chamber RV

A
  • Aberrant hypertrophied muscular bands divide RV in 2 chambers:
    o Proximal high-pressure chamber
    o Distal low-pressure chamber
  • PG is between the inflow and outflow portion of the RV
    o KT advanced from high-pressure chamber → low pressure chamber
    o P in distal chamber = PAP
18
Q

How would you estimate the effective orifice area of a stenotic lesion in the cath lab

A
  • Requires simultaneous measurements of pressure and flow across valve
    o CO
    o Diastolic time if AV valve, systolic time if GA valve
    o HR
    o C is a constant
     MV: 0.85
     AoV, PV, TV: 1
    o PG across valve

Area= (CO/(diastolic or systolic time)(HR) )/(44.3C√PG)