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Invasive Hemodynamics
Kerolus Shehata, MD
Outline
• Cath lab math
• Flows
• Pressure, Resistance
• Shunts
• Stenotic and regurgitant
valves
• PV loops
When Do We Use Invasive Hemodynamics
• When non-invasive assessments are non-diagnostic.
• When there is a discrepancy between clinical and echocardiographic
assessments.
• To evaluate effects of percutaneous therapies intra-procedurally (e.g.
change in LA pressures after TEER; LV-Ao gradient after TAVR).
Tips and Tricks
• Pressure may not reflect true flow if vascular impedance is abnormal.
• Meticulous technique for hemodynamic system.
• Balance and calibrate.
• Systolic pressure amplification, mean pressure may be more accurate.
• Recording artifacts Underdamping & Overdamping.
• Respiratory variation, PEEP, Mechanical ventilation.
• We measure: Pressures, saturations, blood gases.
• We calculated: Flows, resistances and gradients.
Cath Lab Math – Practical tips
• Eliminate technical errors in set up (Damping, bubbles).
• Understand vagaries of CO determinations.
• Understand what flows to use for valve area calculations.
• Understand low output/low gradient AS hemodynamics.
• Recall significant stenotic valve gradients.
• Use Hakki formula for quick valve area calculations.
• Use shunt shortcuts for Qp/Qs calculations.
Important Hemodynamics - RIGHT HEART
• RAP +/or CVP (0-8 mmHg)
• RV Systolic/Diastolic (15-30/0-8 mmHg)
• PA Systolic/Diastolic (15-30/8-12 mmHg)
• SVO2 (70-75%)
• Right heart pumps against PVR (120-250 dynes*sec/cm-5) =
80*(mean PA-PCWP)/CO
• PAPi (>0.9) = (PASP-PADP)/CVP
Important Hemodynamics - LEFT HEART
• PCWP = 5. Left atrial Pressure (8-12 mmHg)
• LVEDP (5-12 mmHg)
• CO (4-7 L/min) via thermodilution (TD) or CCO PA Catheter
• Blood Pressure (100-140/60-90 mmHg)
• MAP (70-100 mmHg)=2/3*Diastolic Pressure + 1/3*Systolic Pressure
• CO (4-7L/min)= FICK equation = (BSA ×120)/ 0.1 × 1.36 × (SaO2-SvO2) × Hgb
• CI (2.5-4.5L/min/m²) = CO/BSA
• L Heart pumps against the SVR (SVR 800-1200dynes*sec/cm-5) = 80* (MAP-
CVP)/CO
• CPO (>1.0 Watts) = (CO x MAP)/451
Cardiac Output
• Cardiac Output = Heart Rate x Stroke Volume (L/min).
• The volume of blood ejected by the heart in a minute.
• Can be measured in several ways: Thermodilution, Fick Method or CMR.
Fick principle
• Described in 1870
• Assumes rate of O2 consumption is a function of rate of blood flow x rate of O2 pick up by RBC
• CO = [MVO2 ] / [AV O2 difference]
• AV O2 difference = Arterial O2 content- Venous O2 content
• O2 content= Hgb x 1.36 x 10 x %O2 sat
• Most accurate at low outputs, steady state
• Large errors possible with small differences in saturations and hemoglobin
• Total error ~ 10-15%
• A-V O2 difference = Arterial O2 content- Venous O2 content
• O2 content= Hgb x 13.6 x %O2 sat
• A-V O2 difference = [O2 content] x [Art sat- Venous sat]
• The larger the A-V O2 difference, the lower the CO
• Normal CO: PA sat 70-80%
• Low CO: PA sat < 65%
• High CO (or L-R shunt): PA sat >80%
Oxygen consumption (VO2)
• Measure of the volume of oxygen used by the body in a minute
• Dependent on the product of oxygen delivery and extraction
• Direct measurement requires mass spectrometry of exhaled air or
a breath-by-breath analysis with a metabolic cart
• Estimated value assumes HR, oxygen delivery and extraction are
stable
• Significant variance in smaller or obese individuals
Thermodilution
• Indicator dilution methods (dye, temperature).
• Most accurate in high output states.
• Less accurate in low output states.
• Inaccurate with TR, AF.
• Variability 15-20%.
Cardiac Power Output (CPO)
• Assesses left heart contractility (flow and SVR)
• CPO = MAP x CO/451
• CPO (normal) = (93x5)/451 = approximately 1.0 Watts
• CPO < 0.6 Watts (0.53) associated with increased mortality
Pulmonary Arterial Pulsatility Index (PAPi)
• Assesses right heart function
• PAPi = PA(systolic) – PA(diastolic)/RA
• PAPi (normal) (25-8)/4 = approx. 4.0
• PAPi < 0.9 associated with RV compromise and need for RV support
• Right Heart Dysfunction: PAPi < 0.9, CVP > 15 mmHg, CVP/PCWP >
0.63, CI < 2.2 L/min/M2 with Left support
Cardiogenic Shock Criteria
• SBP < 90 mmHg for > 30 minutes (or inotropes/vasopressors
to maintain SBP >90)
• Evidence of end-organ hypoperfusion
• Lactate > 2 mmol/L
• Fick CI < 1.8 L/min/m2 w/o inotropes/vasopressors or <2.2
with inotropes/vasopressors
• PCWP > 15 mmHg (18); RVEDP > 10-15 mmHg
• Cardiac Power Output (CPO) < 0.6 Watts
• Pulmonary Arterial Pulsatility Index (PAPi) < 0.9
RA/LA Pressure Wave Forms
• a=atrial contraction; x descent
• c=systolic bulge of TV into RA
• v=atrial filling; y descent
• Measure mean Pressure
• Right-sided: a>v, Left-sided: v>a
PCW Tracing “v” Waves • MR
• VSD
• Noncompliant LA
Pericardial Tamponade • Rapid X only
• No early diastolic RV filling
Before and after pericardiocentesis
Pericardial Constriction • Rapid Y
• Early rapid diastolic RV filling) + Rapid X
Tamponade vs constrictive physiology
Constrictive physiology & RA pressure waveforms
Constriction/Restriction
Constrictive Vs Restrictive hemodynamics
Systolic Discordance
Systolic Concordance
Vascular Resistance
• Resistance = ΔP/CO
• SVR = (mAP - mRAP) x 80/CO. Normal range 700-1600 dynes-sec/cm5
• PVR = (mPA - mPCW) x 80/CO. Normal range 20-130 dynes-sec/cm5
• For Woods Units, divide metric units by 80
O2 Saturations: Intracardiac Shunt
When is A Step-Up Significant?
Location Max Step-up Mean Step-up Shunt Detection
• VC to RA >11 >7 1.5-1.9
• RA to RV >10 >5 1.3-1.5
• RV to PA >5 >5 1.3-1.5
Basics of shunt studies
• No L-R shunt: mixed venous = PA sat
• With L-R shunt, mixed venous O2 sat = O2 sat in chamber proximal to shunt
• For ASD, mixed venous = caval O2 sat = (3xSVC +1xIVC)/4
• No R-L shunt: PV O2 sat= FA O2 sat
• Shunt calculation depends on ratio of total pulmonary blood flow to total
systemic blood flow
• Shunt ratio = Qp /Qs
• Blood flows (pulmonary and systemic) are determined using the Fick equations
Quick Qp/Qs calculation using only Oxygen saturation values
Bidirectional shunts
• Effective blood flow = Qeff = O2 consumption/(PV O2- MVO2)
• Left to right shunt: Qp-Qeff
• Right to left shunt: Qs-Qeff
Can I close this shunt?
• Take away “pop-off” to force full cardiac output across stenotic
valve and/or stiff ventricle
• PA/IVS with antegrade blood flow and ASD: Evaluate TS, RV
compliance, cardiac output
• MS, small left heart sided structures and ASD: Evaluate MS, LV
compliance, LVOT. Be mindful of LA HTN
• Technique: Two venous lines are ideal. Monitor atrium, ventricle,
cardiac output and systemic BP.
AS - Methods of Invasive Evaluation
Method Consideration
• Single catheter LV-aortic pullback Qualitative only; Does not allow for
quantitative calculations
• LV catheter through arterial sheath Use longest sheath possible due to delay
between central and peripheral pressures
• Double arterial access with 2 pigtails Double arterial access
• Double-lumen pigtail catheter Hard to find
• Mother-child aortic guide catheter with smaller pigtail to LV Consider 2Fr system difference or sidehole
guide to avoid dampening of pressure
• Transseptal puncture to access LV with second catheter in aorta Only consider for mechanical AVR
• Guide catheter in aorta with 0.014 pressure wire in LV Cost is higher
• Dual sensor pressure guidewire Cost is even higher
AS hemodynamics
• Aortic Pressure: Delayed
rise in aortic pressure
compared with LV
pressure. Loss of dicrotic
notch
• LV Pressure: LVEDP
commonly elevated. May
see prominent “a” wave
during diastole.
Aortic Valve Area
• Mean AV Gradient: Requires simultaneous LV-Ao pressures
• Aortic Valve Area: Requires LV-Ao gradient and Cardiac Output (e.g. RHC)
• Gorlin equation: AVA = Cardiac output ÷ (44.3 x Heart rate x Systolic ejection period
x Sq rt mean systolic pressure gradient)
• Assumes steady state and fixed orifice
• Not accurate with concomitant regurgitation
• Not accurate at low output
• Not accurate at low or high HR
• For both Aortic and Mitral Valve Area calculations, it’s fine to use the Hakki formula.
• Valve Area= CO/√(mean gradient)
AVA calculation in a nutshell
Peripheral Overshoot • Peak Systolic Pressures are not equal
and do not occur at the same time
Determining AVA when other valvular lesions are present
Distinguishing LFLG-AS from Pseudo-AS
Dobutamine Challenge
AS Vs HOCM
Valsalva After VPB
Gradient Pulse pressure Gradient Pulse pressure
• AS Decrease Decrease Increase Increase
• HOCM Increase Decrease Increase Decrease
• Fixed Valvular AS: Parvus et Tardus in Aortic pressure upstroke.
• HCM: Aortic pressure rises rapidly and then develops spike-and-
dome contour, Late peak of LV Pressure.
Distinguishing AS from HCM: Post-PVC Waveforms
• Post-PVC potentiation increases LV contractility
• AS: Increase in pulse pressure
• HCM: Decrease in pulse pressure due to increase in SAM and outflow
obstruction (Brockenbrough-Braunwald-Morrow Sign).
Postextrasystolic Pulse Pressure in AS
Brockenbrough Sign
Mitral Stenosis
What Information Are We Looking For?
• Mean MV Gradient: Requires simultaneous LA-LV pressures
• MVG simplified=mean LAP −(LVEDP/2)
• Remember that MVG is dependent on heart rate
• Higher HR = less LA emptying = Higher MVG
• Mean MVG measured during diastole by the simultaneous
comparison of LV pressure and LA pressure.
• Simple MVG equation doesn’t require simultaneous
recording of LV/LA diastolic pressures. But this method is
limited if pt is tachycardic, which can reduce accuracy of
LVEDP estimate and overestimate the gradient. And this
makes sense.
• HR effect on MVG is important and the gradient will be
higher with a faster heart rate because there is less time
available for left atrial emptying with a reduced diastolic
period.
Mitral Stenosis
• Gorlin formula best applied to patients in sinus rhythm with normal LV function, no MR, and no other
concomitant valve lesions
• CO=4.2L/min, HR 70, DFP 0.42, Mean Gradient 25, MVA ~4/5 ~ 0.8cm2
PCW does not always equal LA
Usually use PCWP in place of direct LA pressure. And although mean PCWP will usually reflect the mean LAP, the PCWP/LV
pressure gradient frequently overestimates the true severity of mitral stenosis due to phase shift in the PCWP and a delay in
transmission of the change in pressure contour through the pulmonary circulation. So, you can get a 30-50% overestimation
of the true gradient when conventional catheters are used even if you correct for phase shift. You can reduce this
overestimation by confirming that the catheter is truly wedged by checking oxygen sats in the PCWP blood. Direct LA
pressure can be obtained via a transseptal approach. So really you have to decide what therapeutic decision is being made
based on this data and thus how accurate it needs to be.
MVA calculation in a nutshell
Aortic Regurgitation Waveforms
• Ao: rapid upstroke due to augmented LV
contractility and increased systolic pressure
due to increased stroke volume. Rapid fall in
pressure results from regurgitation – results
in widened pulse pressure
• LV: near equalization of Ao and LV pressures
because of continuous leaking of blood back
into the LV producing a rapid rise in LV
pressure across diastole.
Provoked Hemodynamics Tips
• Test occlude everything.
• Second venous line is helpful.
• Think about the rhythm (get into routine of checking before/during
hemodynamics) and pacemaker (if applicable).
Vasodilator testing for pulmonary hypertension
• Indication: Known PH or pulmonary vascular resistance ≥ 3 iWU or Single
ventricles with transpulmonary gradient > 6 mmHg.
• Therapies: Oxygen, inhaled nitric oxide, epoprostenol, iloprost.
• Reactivity: Mean PAP decrease at least 10 and to a value of less than 40 with
increased or unchanged cardiac output and no significant change in systemic
blood pressure. Reduction in PVR by 20%. ID those who may respond to
calcium channel blockers.
• Caution: May cause pulmonary edema in those with LA HTN (or occult PVOD).
Fontan Fenestration test occlusion
• Indication: Electively after fenestrated Fontan or if cyanosis, particularly with
exercise.
• Technique: Doable with one venous access, easier with two.
• Measurements: SvO2, AO sat, Fontan pressure, systemic blood pressure.
• One access: test occlude with Berman or balloon with long sheath in baffle.
• Two access: test occlude with anything, 2nd line measures pressure/obtains
true SvO2.
• Interpretation: Ok to close if no more than 15% change in Fontan pressure,
cardiac output, systemic blood pressure.
Provocable Gradient: Valsalva Maneuver
HOCM: Left heart pullback
Factors influencing LVOT gradient in HOCM
• Higher: Increased contractility, decreased preload, decreased afterload,
volume depletion.
• Lower: Decreased contractility, increased preload, increased afterload.
Significant gradients
Lesion mPG Area
• AS =>40 <=1
• MS >10 <1.5
• PS >40 N/A
• TS >5 N/A
• Ao coarctation P-P >20 N/A
• Subaortic membrane >30 N/A
Regurgitant Volume (MR)
• LV Gram: Total SV = LVEDV-LVESV
• Fick CO/HR= Forward Stroke Volume (FSV)
• RV=TSV-FSV
• RF=RSV/TSV
• Q Total LV = Q Syst + Q RV
• Régurgitant fraction % = Q RV/Q Total LV x100
Estimating valvular regurgitation severity
Chronic Mitral Regurgitation Waveforms
• Left Atrium (or PCWP): Tall V wave. Sensitive, but not
specific marker. Mean pressure may be normal in setting
of compliant LA
• Left Ventricle: Systolic/diastolic pressures often normal
or only slightly increased.
• V waves frequently associated with VSD, or other
disorders associated with altered compliance and
pressure/volume relationships within atrial/ventricular
chambers
• Chronic MR LA: LV and LA directly communicate during
systole, but mean LAP may be normal/slightly increased
due to compliant LA, which dilates in response to
volume overload. Thus, amplitude of V wave is less
than LV systole
• LV pressure: LV is volume overloaded, but LV
compliancy increases so pressures remain normal
Acute Mitral Regurgitation Waveforms
• LA (or PCWP): Tall V wave with amplitude nearly equivalent to
LV systolic pressure
• LV : Diastolic pressures increased due to non-compliance of LV
• In contrast, in acute MR, LV and LA have not had time to adapt
to volume overload. Compliance in both chambers is low. So,
with onset of systole and large volume of regurgitant blood
flow, LAP rises abruptly, and you get a very tall V wave. The
pressure gradient between A ad LV declines by end of systole
so amplitude of V wave and that of LV systole are nearly
equivalent. LVEDP is also elevated because of increase in EDV
within un-dilated and non-compliant chamber
A 70 y/o man with MR
LV gram EDV 120 cc, ESV 30 cc, CO 6.0 L/m, HR 100 bpm
• Total volume: EDV – ESV 120-30=90cc
• Forward volume: Fick CO/HR 6000/100 = 60 cc
• RV = TV – FV = 90 – 60 cc = 30 cc
• RF = RV/TV = 30cc/90cc = 33%
LV pressure-volume loop
PV loop - Normal Physiology
PV loop - Systolic dysfunction
PV loop – Diastolic dysfunction
PV loop – Combined systolic and Diastolic dysfunction
65-year-old woman with multi-valvular heart
disease and rapid AF
FA % sat 96%
PA % sat 55%
Thermodilution CO 5.0 L/min
What is the true cardiac output?
A. Normal
B. Low
C. High
D. Cannot tell
What is the likely cause of this finding?
A. Constriction
B. Restriction
C. Tamponade
D. TR
What is the PVR in Wood Units?
Mean RAP = 10 mmHg
mPA= 40 mm Hg
mPCWP = 20 mmHg
FA = 130/82 mmHg
CO = 4.0 L/min
A. Cannot calculate
B. 250
C. 5
D. 3
VSD Shunt Calculation: what is Qp/Qs
RA 48%
PA 79%
FA 93%
A. 1.0
B. 2.1
C. 2.5
D. 3.2
27M with dizziness and systolic murmur
What is the lesion?
A. AS
B. HOCM
C. MR
D. VSD
E. Subaortic membrane
59F with severe DOE
What is the abnormality?
A. ARVD
B. ASD
C. PS
D. Pulmonary hypertension
E. TR
What Valve Lesion is Suggested?
A. MR
B. MS
C. AR
D. AS
E. TR
Interpret the post-TAVR findings
• Ao-LV gradient reduction.
• Improved Ao upslope.
• Widened Ao pulse pressure.
• Rapid LV diastolic filling.
• High LVEDP.
• Matching LVEDP with Ao diastolic
= Acute AI post-TAVR
• Rapid pacing for stabilization
then valve in valve implantation.
What was the procedure?
• No LVOT gradient
• No spike/dome Ao
• RBBB
• LVEDP elevation
Thank You

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Invasive Hemodynamics: Assessment and interpretation

  • 2. Outline • Cath lab math • Flows • Pressure, Resistance • Shunts • Stenotic and regurgitant valves • PV loops
  • 3. When Do We Use Invasive Hemodynamics • When non-invasive assessments are non-diagnostic. • When there is a discrepancy between clinical and echocardiographic assessments. • To evaluate effects of percutaneous therapies intra-procedurally (e.g. change in LA pressures after TEER; LV-Ao gradient after TAVR).
  • 4. Tips and Tricks • Pressure may not reflect true flow if vascular impedance is abnormal. • Meticulous technique for hemodynamic system. • Balance and calibrate. • Systolic pressure amplification, mean pressure may be more accurate. • Recording artifacts Underdamping & Overdamping. • Respiratory variation, PEEP, Mechanical ventilation. • We measure: Pressures, saturations, blood gases. • We calculated: Flows, resistances and gradients.
  • 5. Cath Lab Math – Practical tips • Eliminate technical errors in set up (Damping, bubbles). • Understand vagaries of CO determinations. • Understand what flows to use for valve area calculations. • Understand low output/low gradient AS hemodynamics. • Recall significant stenotic valve gradients. • Use Hakki formula for quick valve area calculations. • Use shunt shortcuts for Qp/Qs calculations.
  • 6. Important Hemodynamics - RIGHT HEART • RAP +/or CVP (0-8 mmHg) • RV Systolic/Diastolic (15-30/0-8 mmHg) • PA Systolic/Diastolic (15-30/8-12 mmHg) • SVO2 (70-75%) • Right heart pumps against PVR (120-250 dynes*sec/cm-5) = 80*(mean PA-PCWP)/CO • PAPi (>0.9) = (PASP-PADP)/CVP
  • 7. Important Hemodynamics - LEFT HEART • PCWP = 5. Left atrial Pressure (8-12 mmHg) • LVEDP (5-12 mmHg) • CO (4-7 L/min) via thermodilution (TD) or CCO PA Catheter • Blood Pressure (100-140/60-90 mmHg) • MAP (70-100 mmHg)=2/3*Diastolic Pressure + 1/3*Systolic Pressure • CO (4-7L/min)= FICK equation = (BSA ×120)/ 0.1 × 1.36 × (SaO2-SvO2) × Hgb • CI (2.5-4.5L/min/m²) = CO/BSA • L Heart pumps against the SVR (SVR 800-1200dynes*sec/cm-5) = 80* (MAP- CVP)/CO • CPO (>1.0 Watts) = (CO x MAP)/451
  • 8. Cardiac Output • Cardiac Output = Heart Rate x Stroke Volume (L/min). • The volume of blood ejected by the heart in a minute. • Can be measured in several ways: Thermodilution, Fick Method or CMR.
  • 9. Fick principle • Described in 1870 • Assumes rate of O2 consumption is a function of rate of blood flow x rate of O2 pick up by RBC • CO = [MVO2 ] / [AV O2 difference] • AV O2 difference = Arterial O2 content- Venous O2 content • O2 content= Hgb x 1.36 x 10 x %O2 sat • Most accurate at low outputs, steady state • Large errors possible with small differences in saturations and hemoglobin • Total error ~ 10-15% • A-V O2 difference = Arterial O2 content- Venous O2 content • O2 content= Hgb x 13.6 x %O2 sat • A-V O2 difference = [O2 content] x [Art sat- Venous sat] • The larger the A-V O2 difference, the lower the CO • Normal CO: PA sat 70-80% • Low CO: PA sat < 65% • High CO (or L-R shunt): PA sat >80%
  • 10. Oxygen consumption (VO2) • Measure of the volume of oxygen used by the body in a minute • Dependent on the product of oxygen delivery and extraction • Direct measurement requires mass spectrometry of exhaled air or a breath-by-breath analysis with a metabolic cart • Estimated value assumes HR, oxygen delivery and extraction are stable • Significant variance in smaller or obese individuals
  • 11. Thermodilution • Indicator dilution methods (dye, temperature). • Most accurate in high output states. • Less accurate in low output states. • Inaccurate with TR, AF. • Variability 15-20%.
  • 12. Cardiac Power Output (CPO) • Assesses left heart contractility (flow and SVR) • CPO = MAP x CO/451 • CPO (normal) = (93x5)/451 = approximately 1.0 Watts • CPO < 0.6 Watts (0.53) associated with increased mortality
  • 13. Pulmonary Arterial Pulsatility Index (PAPi) • Assesses right heart function • PAPi = PA(systolic) – PA(diastolic)/RA • PAPi (normal) (25-8)/4 = approx. 4.0 • PAPi < 0.9 associated with RV compromise and need for RV support • Right Heart Dysfunction: PAPi < 0.9, CVP > 15 mmHg, CVP/PCWP > 0.63, CI < 2.2 L/min/M2 with Left support
  • 14. Cardiogenic Shock Criteria • SBP < 90 mmHg for > 30 minutes (or inotropes/vasopressors to maintain SBP >90) • Evidence of end-organ hypoperfusion • Lactate > 2 mmol/L • Fick CI < 1.8 L/min/m2 w/o inotropes/vasopressors or <2.2 with inotropes/vasopressors • PCWP > 15 mmHg (18); RVEDP > 10-15 mmHg • Cardiac Power Output (CPO) < 0.6 Watts • Pulmonary Arterial Pulsatility Index (PAPi) < 0.9
  • 15. RA/LA Pressure Wave Forms • a=atrial contraction; x descent • c=systolic bulge of TV into RA • v=atrial filling; y descent • Measure mean Pressure • Right-sided: a>v, Left-sided: v>a
  • 16. PCW Tracing “v” Waves • MR • VSD • Noncompliant LA
  • 17. Pericardial Tamponade • Rapid X only • No early diastolic RV filling
  • 18. Before and after pericardiocentesis
  • 19. Pericardial Constriction • Rapid Y • Early rapid diastolic RV filling) + Rapid X
  • 21. Constrictive physiology & RA pressure waveforms
  • 26. Vascular Resistance • Resistance = ΔP/CO • SVR = (mAP - mRAP) x 80/CO. Normal range 700-1600 dynes-sec/cm5 • PVR = (mPA - mPCW) x 80/CO. Normal range 20-130 dynes-sec/cm5 • For Woods Units, divide metric units by 80
  • 28. When is A Step-Up Significant? Location Max Step-up Mean Step-up Shunt Detection • VC to RA >11 >7 1.5-1.9 • RA to RV >10 >5 1.3-1.5 • RV to PA >5 >5 1.3-1.5
  • 29. Basics of shunt studies • No L-R shunt: mixed venous = PA sat • With L-R shunt, mixed venous O2 sat = O2 sat in chamber proximal to shunt • For ASD, mixed venous = caval O2 sat = (3xSVC +1xIVC)/4 • No R-L shunt: PV O2 sat= FA O2 sat • Shunt calculation depends on ratio of total pulmonary blood flow to total systemic blood flow • Shunt ratio = Qp /Qs • Blood flows (pulmonary and systemic) are determined using the Fick equations
  • 30. Quick Qp/Qs calculation using only Oxygen saturation values
  • 31. Bidirectional shunts • Effective blood flow = Qeff = O2 consumption/(PV O2- MVO2) • Left to right shunt: Qp-Qeff • Right to left shunt: Qs-Qeff
  • 32. Can I close this shunt? • Take away “pop-off” to force full cardiac output across stenotic valve and/or stiff ventricle • PA/IVS with antegrade blood flow and ASD: Evaluate TS, RV compliance, cardiac output • MS, small left heart sided structures and ASD: Evaluate MS, LV compliance, LVOT. Be mindful of LA HTN • Technique: Two venous lines are ideal. Monitor atrium, ventricle, cardiac output and systemic BP.
  • 33. AS - Methods of Invasive Evaluation Method Consideration • Single catheter LV-aortic pullback Qualitative only; Does not allow for quantitative calculations • LV catheter through arterial sheath Use longest sheath possible due to delay between central and peripheral pressures • Double arterial access with 2 pigtails Double arterial access • Double-lumen pigtail catheter Hard to find • Mother-child aortic guide catheter with smaller pigtail to LV Consider 2Fr system difference or sidehole guide to avoid dampening of pressure • Transseptal puncture to access LV with second catheter in aorta Only consider for mechanical AVR • Guide catheter in aorta with 0.014 pressure wire in LV Cost is higher • Dual sensor pressure guidewire Cost is even higher
  • 34. AS hemodynamics • Aortic Pressure: Delayed rise in aortic pressure compared with LV pressure. Loss of dicrotic notch • LV Pressure: LVEDP commonly elevated. May see prominent “a” wave during diastole.
  • 35. Aortic Valve Area • Mean AV Gradient: Requires simultaneous LV-Ao pressures • Aortic Valve Area: Requires LV-Ao gradient and Cardiac Output (e.g. RHC) • Gorlin equation: AVA = Cardiac output ÷ (44.3 x Heart rate x Systolic ejection period x Sq rt mean systolic pressure gradient) • Assumes steady state and fixed orifice • Not accurate with concomitant regurgitation • Not accurate at low output • Not accurate at low or high HR • For both Aortic and Mitral Valve Area calculations, it’s fine to use the Hakki formula. • Valve Area= CO/√(mean gradient)
  • 36. AVA calculation in a nutshell
  • 37. Peripheral Overshoot • Peak Systolic Pressures are not equal and do not occur at the same time
  • 38. Determining AVA when other valvular lesions are present
  • 39. Distinguishing LFLG-AS from Pseudo-AS Dobutamine Challenge
  • 40. AS Vs HOCM Valsalva After VPB Gradient Pulse pressure Gradient Pulse pressure • AS Decrease Decrease Increase Increase • HOCM Increase Decrease Increase Decrease • Fixed Valvular AS: Parvus et Tardus in Aortic pressure upstroke. • HCM: Aortic pressure rises rapidly and then develops spike-and- dome contour, Late peak of LV Pressure.
  • 41. Distinguishing AS from HCM: Post-PVC Waveforms • Post-PVC potentiation increases LV contractility • AS: Increase in pulse pressure • HCM: Decrease in pulse pressure due to increase in SAM and outflow obstruction (Brockenbrough-Braunwald-Morrow Sign).
  • 44. Mitral Stenosis What Information Are We Looking For? • Mean MV Gradient: Requires simultaneous LA-LV pressures • MVG simplified=mean LAP −(LVEDP/2) • Remember that MVG is dependent on heart rate • Higher HR = less LA emptying = Higher MVG • Mean MVG measured during diastole by the simultaneous comparison of LV pressure and LA pressure. • Simple MVG equation doesn’t require simultaneous recording of LV/LA diastolic pressures. But this method is limited if pt is tachycardic, which can reduce accuracy of LVEDP estimate and overestimate the gradient. And this makes sense. • HR effect on MVG is important and the gradient will be higher with a faster heart rate because there is less time available for left atrial emptying with a reduced diastolic period.
  • 45. Mitral Stenosis • Gorlin formula best applied to patients in sinus rhythm with normal LV function, no MR, and no other concomitant valve lesions • CO=4.2L/min, HR 70, DFP 0.42, Mean Gradient 25, MVA ~4/5 ~ 0.8cm2
  • 46. PCW does not always equal LA Usually use PCWP in place of direct LA pressure. And although mean PCWP will usually reflect the mean LAP, the PCWP/LV pressure gradient frequently overestimates the true severity of mitral stenosis due to phase shift in the PCWP and a delay in transmission of the change in pressure contour through the pulmonary circulation. So, you can get a 30-50% overestimation of the true gradient when conventional catheters are used even if you correct for phase shift. You can reduce this overestimation by confirming that the catheter is truly wedged by checking oxygen sats in the PCWP blood. Direct LA pressure can be obtained via a transseptal approach. So really you have to decide what therapeutic decision is being made based on this data and thus how accurate it needs to be.
  • 47. MVA calculation in a nutshell
  • 48. Aortic Regurgitation Waveforms • Ao: rapid upstroke due to augmented LV contractility and increased systolic pressure due to increased stroke volume. Rapid fall in pressure results from regurgitation – results in widened pulse pressure • LV: near equalization of Ao and LV pressures because of continuous leaking of blood back into the LV producing a rapid rise in LV pressure across diastole.
  • 49. Provoked Hemodynamics Tips • Test occlude everything. • Second venous line is helpful. • Think about the rhythm (get into routine of checking before/during hemodynamics) and pacemaker (if applicable).
  • 50. Vasodilator testing for pulmonary hypertension • Indication: Known PH or pulmonary vascular resistance ≥ 3 iWU or Single ventricles with transpulmonary gradient > 6 mmHg. • Therapies: Oxygen, inhaled nitric oxide, epoprostenol, iloprost. • Reactivity: Mean PAP decrease at least 10 and to a value of less than 40 with increased or unchanged cardiac output and no significant change in systemic blood pressure. Reduction in PVR by 20%. ID those who may respond to calcium channel blockers. • Caution: May cause pulmonary edema in those with LA HTN (or occult PVOD).
  • 51. Fontan Fenestration test occlusion • Indication: Electively after fenestrated Fontan or if cyanosis, particularly with exercise. • Technique: Doable with one venous access, easier with two. • Measurements: SvO2, AO sat, Fontan pressure, systemic blood pressure. • One access: test occlude with Berman or balloon with long sheath in baffle. • Two access: test occlude with anything, 2nd line measures pressure/obtains true SvO2. • Interpretation: Ok to close if no more than 15% change in Fontan pressure, cardiac output, systemic blood pressure.
  • 53. HOCM: Left heart pullback
  • 54. Factors influencing LVOT gradient in HOCM • Higher: Increased contractility, decreased preload, decreased afterload, volume depletion. • Lower: Decreased contractility, increased preload, increased afterload.
  • 55. Significant gradients Lesion mPG Area • AS =>40 <=1 • MS >10 <1.5 • PS >40 N/A • TS >5 N/A • Ao coarctation P-P >20 N/A • Subaortic membrane >30 N/A
  • 56. Regurgitant Volume (MR) • LV Gram: Total SV = LVEDV-LVESV • Fick CO/HR= Forward Stroke Volume (FSV) • RV=TSV-FSV • RF=RSV/TSV • Q Total LV = Q Syst + Q RV • Régurgitant fraction % = Q RV/Q Total LV x100
  • 58. Chronic Mitral Regurgitation Waveforms • Left Atrium (or PCWP): Tall V wave. Sensitive, but not specific marker. Mean pressure may be normal in setting of compliant LA • Left Ventricle: Systolic/diastolic pressures often normal or only slightly increased. • V waves frequently associated with VSD, or other disorders associated with altered compliance and pressure/volume relationships within atrial/ventricular chambers • Chronic MR LA: LV and LA directly communicate during systole, but mean LAP may be normal/slightly increased due to compliant LA, which dilates in response to volume overload. Thus, amplitude of V wave is less than LV systole • LV pressure: LV is volume overloaded, but LV compliancy increases so pressures remain normal
  • 59. Acute Mitral Regurgitation Waveforms • LA (or PCWP): Tall V wave with amplitude nearly equivalent to LV systolic pressure • LV : Diastolic pressures increased due to non-compliance of LV • In contrast, in acute MR, LV and LA have not had time to adapt to volume overload. Compliance in both chambers is low. So, with onset of systole and large volume of regurgitant blood flow, LAP rises abruptly, and you get a very tall V wave. The pressure gradient between A ad LV declines by end of systole so amplitude of V wave and that of LV systole are nearly equivalent. LVEDP is also elevated because of increase in EDV within un-dilated and non-compliant chamber
  • 60. A 70 y/o man with MR LV gram EDV 120 cc, ESV 30 cc, CO 6.0 L/m, HR 100 bpm • Total volume: EDV – ESV 120-30=90cc • Forward volume: Fick CO/HR 6000/100 = 60 cc • RV = TV – FV = 90 – 60 cc = 30 cc • RF = RV/TV = 30cc/90cc = 33%
  • 62. PV loop - Normal Physiology
  • 63. PV loop - Systolic dysfunction
  • 64. PV loop – Diastolic dysfunction
  • 65. PV loop – Combined systolic and Diastolic dysfunction
  • 66. 65-year-old woman with multi-valvular heart disease and rapid AF FA % sat 96% PA % sat 55% Thermodilution CO 5.0 L/min What is the true cardiac output? A. Normal B. Low C. High D. Cannot tell
  • 67. What is the likely cause of this finding? A. Constriction B. Restriction C. Tamponade D. TR
  • 68. What is the PVR in Wood Units? Mean RAP = 10 mmHg mPA= 40 mm Hg mPCWP = 20 mmHg FA = 130/82 mmHg CO = 4.0 L/min A. Cannot calculate B. 250 C. 5 D. 3
  • 69. VSD Shunt Calculation: what is Qp/Qs RA 48% PA 79% FA 93% A. 1.0 B. 2.1 C. 2.5 D. 3.2
  • 70. 27M with dizziness and systolic murmur What is the lesion? A. AS B. HOCM C. MR D. VSD E. Subaortic membrane
  • 71. 59F with severe DOE What is the abnormality? A. ARVD B. ASD C. PS D. Pulmonary hypertension E. TR
  • 72. What Valve Lesion is Suggested? A. MR B. MS C. AR D. AS E. TR
  • 73. Interpret the post-TAVR findings • Ao-LV gradient reduction. • Improved Ao upslope. • Widened Ao pulse pressure. • Rapid LV diastolic filling. • High LVEDP. • Matching LVEDP with Ao diastolic = Acute AI post-TAVR • Rapid pacing for stabilization then valve in valve implantation.
  • 74. What was the procedure? • No LVOT gradient • No spike/dome Ao • RBBB • LVEDP elevation