SCAI CHAP 13 Hemodynamics Flashcards

(56 cards)

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Q1. What signals and initiates atrial contraction at the beginning of the cardiac cycle?

Q2. What pressure wave denotes atrial systole?

Q3. What pressure wave denotes atrial diastole?

Q4. Which wave signals depolarization of the ventricles?

Q5. What does the left ventricular end diastolic pressure (LVEDP) correspond to?

Q6. What happens about 15 to 30 ms after the QRS wave?

Q7. When does the aortic valve (AV) open?

Q8. What signals ventricular repolarization?

Q9. When does the aortic valve (AV) close?

Q10. When does the mitral valve (MV) open?

A

A1. The P wave.

A2. The “a” wave.

A3. The “x” descent.

A4. The QRS wave.

A5. The R wave intersection with LV pressure.

A6. Ventricles contract, and LV pressure rises rapidly.

A7. When LV pressure rises above aortic pressure.

A8. The T wave.

A9. When LV pressure falls below aortic pressure.

A10. When LV pressure falls below left atrial pressure.

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Q1. The cardiac cycle begins with the ______ wave, which signals and initiates atrial contraction.

Q2. Atrial systole is denoted as the “______” wave.

Q3. Atrial diastole is denoted as the “______” descent.

Q4. The ______ wave signals depolarization of the ventricles.

Q5. The left ventricular end diastolic pressure (LVEDP) corresponds to the intersection of the ______ wave with LV pressure (point b in fig 1)

Q6. About 15 to 30 ms after the QRS, the ventricles contract and LV pressure increases rapidly during the ______ contraction period.

Q7. The aortic valve (AV) opens when LV pressure rises above ______ pressure.

Q8. Ventricular repolarization is signaled by the ______ wave.

Q9. The aortic valve closes when LV pressure falls below ______ pressure.

Q10. The mitral valve (MV) opens when LV pressure falls below ______ pressure.

Q11. “A/x” pressures, is followed by the ____ , signaling depolarization of the ventricles ( also point b in fig 1) .

Q12. Systolic ejection continues until _________ , signaled by the T wave (point d in fig 1).

Q13. Point e is when _______ closes, the LV pressure falls below the aortic pressures

Q14. Point f in fig 1, is when _____ opens and the LA empties into the LV.

A

A1. P

A2. a

A3. x

A4. QRS

A5. R

A6. isovolumetric ( point b to point c in fig 1 )

A7. aortic

A8. T

A9. aortic

A10. left atrial

A11. QRS

A12. repolarization

A13. Aortic valve

A14. Mitral valve

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Q1. After the “a” wave, atrial pressure slowly ______ with atrial filling during systole.

Q2. Atrial pressure continues to increase until the end of ______.

Q3. At the end of systole, the pressure and volume of the left atrium (LA) are nearly ______.

Q4. The ventricular filling wave produced at the end of systole is called the “______” wave.

Q5. The “v” wave peak ( point 4 in fig 1) is followed by a rapid fall labeled the “______” descent.

Q6. The “Y” descent occurs when the ______ valve opens.

Q7. The peaks and troughs of the atrial pressure waves can be changed by ______ conditions.

Q8. Name one pathologic condition that can change atrial pressure waveforms.

Q9. Another pathologic condition affecting atrial pressure waves is ______.

Q10. Infarction is a pathologic condition that can alter the ______ pressure waveforms.

A

A1. rises

A2. systole

A3. maximal

A4. v ( The v wave is a peak in the atrial pressure curve that occurs during ventricular systole. It represents the increase in atrial pressure due to filling of the atrium while the mitral valve is closed. This wave reflects the accumulation of blood in the left atrium as it fills from the pulmonary veins before the mitral valve opens for ventricular filling.)

A5. Y

A6. mitral

A7. pathologic

A8. acute valvular regurgitation

A9. heart failure

A10. atrial

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Q1. What happens to atrial pressure after the “a” wave?

Q2. Until when does atrial pressure continue to increase?

Q3. What is the state of the left atrium’s pressure and volume at the end of systole?

Q4. What is the name of the ventricular filling wave produced at the end of systole?

Q5. What follows the “v” wave peak?

Q6. When does the “Y” descent occur?

Q7. What can change the peaks and troughs of atrial pressure waves?

Q8. Name a pathologic condition that changes atrial pressure waves.

Q9. Name another pathologic condition affecting atrial pressure waves.

Q10. What kind of pressure waveforms can infarction alter?

A

A1. Atrial pressure slowly rises with atrial filling during systole.

A2. Until the end of systole.

A3. Nearly maximal.

A4. The “v” wave.

A5. A rapid fall labeled the “Y” descent ( The steepness and depth of the Y descent can provide information about right ventricular filling and compliance. A prominent or rapid Y descent may be seen in conditions like constrictive pericarditis or restrictive cardiomyopathy, where the ventricle fills quickly but then is limited by stiff walls.
A blunted or absent Y descent may indicate tricuspid stenosis or impaired right ventricular filling )

A6. When the mitral valve opens.

A7. Pathologic conditions.

A8. Acute valvular regurgitation.

A9. Heart failure.

A10. Atrial pressure waveforms.

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Q1. RA pressure normally ______ with intrathoracic pressure during spontaneous inspiration.

Q2. In patients with congestive heart failure, RA pressure during inspiration may fail to ______.

Q3. RA pressure might even ______ during inspiration in certain conditions.

Q4. One condition causing impaired venous return to the right heart is ______ constriction.

Q5. The sign where RA pressure INCREASES during inspiration is called ______ sign.

Q6. This sign reflects impaired filling of the ______.

Q7. The sign also indicates elevated ______.

Q8. Rapid “Y” descents during inspiration are shown in ______.

Q9. During inspiration, there may be no change in mean ______ pressure.

Q10. Impaired venous return affects the ______ side of the heart.

A

A1. decreases

A2. decrease

A3. increase

A4. pericardial

A5. Kussmaul

A6. right ventricle (RV)

A7. pressures

A8. Fig. 13.4

A9. RA

A10. right

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Q1. How does RA pressure normally change during spontaneous inspiration?

Q2. What happens to RA pressure during inspiration in patients with congestive heart failure?

Q3. What condition can impair venous return to the right side of the heart?

Q4. What happens to RA pressure during inspiration in pericardial constriction?

Q5. What is the name of the sign when RA pressure fails to decrease OR increases during inspiration?

Q6. What does the Kussmaul sign reflect?

Q7. What part of the heart has impaired filling in these conditions?

Q8. What happens to pressures in the right ventricle during impaired filling?

Q9. What does Fig. 13.4 show during inspiration?

Q10. Is there a change in mean RA pressure during inspiration in these patients?

Q11. a wave = ?, x = ? , V=? and y =?

A

A1. RA pressure normally decreases.

A2. RA pressure may fail to decrease or increase ( kussmaul )

A3. Pericardial constriction.

A4. RA pressure may fail to decrease OR increase ( mean RA pressure )

A5. Kussmaul sign.

A6. Impaired filling of the RV and elevated pressures.

A7. Right ventricle (RV).

A8. Pressures are elevated.

A9. Rapid “Y” descents during inspiration (The steepness and depth of the Y descent can provide information about right ventricular filling and compliance. A prominent or rapid Y descent may be seen in conditions like constrictive pericarditis or restrictive cardiomyopathy, where the ventricle fills quickly but then is limited by stiff walls.
A blunted or absent Y descent may indicate tricuspid stenosis or impaired right ventricular filling. )

A10. No change in mean RA pressure.

A11. [ a= atrial systole ], [ x = atrial diastole] , [ v= v wave is a peak in the atrial pressure curve that occurs during ventricular systole. It represents the increase in atrial pressure due to filling of the atrium while the mitral valve is closed. This wave reflects the accumulation of blood in the left atrium as it fills from the pulmonary veins before the mitral valve opens for ventricular filling ], [ y= rapid fall when mitral valve opens ].

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Hints ( me ):

A
  • a wave occurs shortly after p wave ( EKG ) and v wave occurs shortly after QRS.
  • CHF/constrictive pericarditis : RA pressure fails to decrease with inspiration and mean RAP either fails to decrease or it will increase during inspiration ( kussmaul ). This occurs because of higher right chambers pressures and also suggested by a rapid y descent because of the rapid filling of the Right ventricle as RVP ( and RAP) is higher.
  • poor complinace of a chamber = stiff chamber
  • stiff atrium ( poor compliance ) leads to a larger v wave for example.
  • i think if blood flowing TOWARDS a stiff chamber, the corresponding waveform is large e.g. large V wave when the LA is stiff or rapid and deep y descent because of a stiff noncompliant RV.
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Q1. What determines pressure waves in the atria?

Q2. What might a poorly compliant atrial chamber demonstrate despite normal flow?

Q3. How does a very compliant atrial chamber respond in terms of pressure wave changes?

Q4. What condition is associated with a low-compliance left atrium?

Q5. What causes high left atrial pressure in the example given ( fig 13.5) ?

Q6. What does the “v” wave in the left atrial pressure waveform indicate in this example?

Q7. Is the large “v” wave due to mitral regurgitation in this example?

Q8. What arrhythmia is present in the example?

Q9. What wave is absent due to atrial fibrillation?

Q10. What notch is present preceding the large “v” wave in atrial fibrillation?

A

A1. The pressure/flow relationship or compliance of the atrial chamber.

A2. A large “v” wave.

A3. It may not register marked pressure wave changes despite torrential flow.

A4. Mitral stenosis (MS).

A5. Both mitral stenosis and a stiff left atrium after rheumatic inflammation.

A6. It indicates poor compliance of the atrium ( catheter sitting inside the LA showing large v waves due to poor LA compliance, while v wave of the RA pressure is normal )

A7. No, it is not due to regurgitation.

A8. Atrial fibrillation.

A9. The “a” waves.

A10. The “c” notch ( arrhythmia may distort pressure waveform )

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14
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Q1. How do normal RA “a” and “v” waves compare to those in the left atrium?

Q2. What happens to the RA waveforms in significant valve dysfunction?

Q3. What condition causes the RA wave to lose its characteristic “a” and “v” waves?

Q4. What wave replaces the “a” and “v” waves in tricuspid regurgitation?

Q5. What does the “s” wave represent in tricuspid regurgitation?

Q6. What symptom did the 67-year-old woman have in the example fig 13.6 ?

Q7. What physical exam finding did the woman have?

Q8. How does the murmur vary in the woman’s case?

Q9. What does Fig. 13.7A show in the patient with severe tricuspid regurgitation?

Q10. What imaging is shown in Fig. 13.7B?

A

A1. Normal RA “a” and “v” waves are smaller than those in the left atrium.

A2. RA waveforms become distorted.

A3. Tricuspid regurgitation.

A4. A large and broad “s” (systolic) wave.

A5. Blood reflux from the right ventricle back into the right atrium.

A6. Dyspnea at rest.

A7. Systolic murmur.

A8. The murmur varies with respiration.

A9. The corresponding pattern of right ventricular and right atrial pressures.

A10. Right ventricular angiogram.

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q1: The pressure-volume (PV) loop plots changes in ______ and ______ over a cardiac cycle.

q2: The shape of the PV loop is specific for the ventricle/______ circuit coupling.

q3: The PV loop for the left ventricle/aorta is different from the PV loop for the right ventricle/______ artery.

q4: The PV loop represents one complete ______ cycle.

q5: At end-diastole (point a), left ventricular (LV) volume is ______ because it has received the atrial contribution.

q6: During isovolumic contraction (from point “a” to “b”), LV pressure ______ while LV volume remains ______.

q7: At the end of isovolumic contraction, the aortic valve (AV) opens when LV pressure exceeds ______ pressure.

q8: Blood is ejected from the LV into the aorta at point ______ on the PV loop.

q9: Over the systolic ejection phase, LV volume decreases, and as ventricular repolarization occurs, LV ejection ceases and relaxation begins. The end-systolic pressure-volume point (ESPV) corresponds to the point where the aortic valve ______.

q10: Isovolumic relaxation occurs after the aortic valve closes until LV pressure falls below ______ pressure.

q11: The mitral valve (MV) opens at point ______ on the PV loop.

A

a1: pressure and volume

a2: arterial

a3: pulmonary

a4: cardiac

a5: maximal

a6: increases; unchanged

a7: aortic

a8: b

a9: closes

a10: atrial

a11: d

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Q1: What does the width of the PV loop represent?

Q2: What is the difference between in stroke volume calculation?

Q3: What does the area within the PV loop represent?

Q4: What is load-independent LV contractility also called?

Q5: What defines load independant LV contractility ?

Q6: What does effective arterial elastance (Ea) measure?

Q7: How is Ea calculated?

Q8: When does optimal LV contractile efficiency occur?

Q9: What properties does the PV loop describe?

Q10: Why are PV loops useful in comparing hemodynamic interventions?

A

A1: Stroke volume (SV)

A2: End-systolic volume and end-diastolic volume

A3: Stroke work

A4: Emax

A5: The line of maximal slopes of ESPV points under varying loads

A6: LV afterload

A7: Ratio of end-systolic pressure to stroke volume

A8: When Ea:Emax ratio approaches 1

A9: Contractile function, relaxation properties, SV, cardiac work, myocardial oxygen consumption

A10: They show predictable changes in PV relationships for precise comparisons

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21
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CHANGES IN PRELOAD:

A
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22
Q

CHANGES IN AFTERLOAD ( TVR ) OR CONTRACTILITY : ( USUALLY BOTH DO NOT AFFECT MUCH LVEDP )

A
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23
Q

FOR THE WAVEFOMRS ABOVE: THINK PHYSIOLOGY AND WHAT MAKES SENSE THEN INTERPRET EACH WAVEFORM.

NEXT SLIDE : WHAT HAPPENS WHEN YOU !!DECREASE!! LV CONTRACTILITY LIKE IN AMI OR SCHOCK ??

A

E.G. IF I INCREASE LV CONTRACTILITY ( SLOPE ), I EXPECT SV TO INCREASE ( CORRELATE THIS WITH WHAT YOU SEE IN THE WAVEFORM )

NEXT SLIDE : WHAT HAPPENS WHEN YOU !!DECREASE!! LV CONTRACTILITY LIKE IN AMI OR SCHOCK ??

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Q

q1: What happens to LV contractility (Emax) in acute myocardial infarction?

q2: How does LV pressure change in acute myocardial infarction?

q3: What may happen to stroke volume (SV) in acute myocardial infarction?

q4: What happens to LV end-diastolic pressure (LVEDP) in acute myocardial infarction?

q5: How is Emax affected in cardiogenic shock?

q6: What may happen to LV afterload (Ea) in cardiogenic shock?

q7: What happens to LV end-diastolic volume (LVEDV) in cardiogenic shock?

q8: How is stroke volume (SV) affected in cardiogenic shock?

q9: What does cardiogenic shock display in terms of LV function?

q10: What happens to LVEDP in cardiogenic shock?

q11: How does myocardial oxygen demand change in cardiogenic shock?

q12: What characterizes severe myocardial infarction evolving into cardiogenic shock?

A

a1: It is reduced

a2: It may be unchanged or reduced

a3: It may be unchanged or reduced

a4: It is increased!

a5: It is severely reduced

a6: the arterial elastance Ea may be increased

a7: It is increased

a8: It is reduced

a9: Reduced LV contractile function and acute diastolic dysfunction

a10: It is increased

a11: It is increased

a12: Markedly reduced SV and significant increases in end-diastolic pressure and volume

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Ees ( end systolic elastance ) is DIFFERENT than Eas ( effective arterial elastance ) and also DIFFERENT than Emax ( load independant LV contractility ). ESPVR is approximately linear with slope end-systolic elastance (Ees) and volume-axis intercept (Vo). Effective arterial elastance (Ea) ( ratio ESP/SV ) is a measure of LV afterload and is the slope of the line extending from the end-diastolic volume (EDV) point on the volume axis through the end-systolic pressure-volume point of the loop. E max or Load-independent LV contractility, is defined as the maximal slope of the end-systolic pressure volume (ESPV) point under various loading conditions, known as the ESPV relationship (ESPVR).
A: Normal PVL, is bounded by the end-systolic pressure-volume relationship (ESPVR) and end-diastolic pressure-volume relationship (EDPVR). !!! ESPVR ( relationship line ) is approximately linear with slope end-systolic elastance (Ees) and volume-axis intercept (Vo). V0 is close to zero but not equal to zero. !!!! Effective arterial elastance (Ea) ( ratio ESP/SV ) is a measure of LV afterload and is the slope of the line extending from the end-diastolic volume (EDV) point on the volume axis through the end-systolic pressure-volume point of the loop. !!!! B: Slope of the Ea line depends on total peripheral resistance (TPR) and heart rate (HR), and its position depends on EDV. C: ESPVR shifts with changes in ventricular contractility, which can be a combination of changes in Ees and Vo. Changes in contractility can be indexed by V120, the volume at which the ESPVR intersects 120 mm Hg. !!!Load-independent LV contractility also known as Emax, is defined as the maximal slope of the end-systolic pressure volume (ESPV) point under various loading conditions, known as the ESPV relationship (ESPVR). !!!Effective arterial elastance (Ea) is a measure of LV afterload and is defined as the ratio of end-systolic pressure and stroke volume. ESV, end-systolic volume; LV, left ventricular.
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Q1: Prior to birth, left atrial (LA) pressure remains ______ relative to right atrial (RA) pressure due to fetal circulation dynamics. Q2: The transition at birth involves lung expansion , which alters intracardiac ____ . Q3: The elevated flow from _______ post-birth increases LA pressure sufficiently to functionally close the . Q4: Postnatally, the RA and RV are exposed to a lower vascular resistance characteristic of the ______ circulation. Q5: Conversely, the LA and LV encounter greater afterload imposed by the ______ circulatory system. Q6: In aortic stenosis, transseptal pressure pullback reveals prominent LA ______ waves, indicative of elevated atrial pressure. Q7: Correspondingly, in aortic stenosis, the RA exhibits attenuated ______ and “v” waves due to impaired filling dynamics. Q8: The Valsalva maneuver transiently reverses atrial pressure gradients, causing RA pressure to exceed LA pressure and potentially precipitate right-to-left ______. Q9: The presence of a patent foramen ovale (PFO) facilitates paradoxical embolism through this abnormal ______ shunt.
A1: lower A2: pressure gradients A3: the right ventricle, PFO A4: pulmonary A5: systemic A6: v A7: a A8: shunting A9: interatrial
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Q1: Percutaneous closure of ______ and ______ are routinely performed in many laboratories by experienced operators. Q2: Patent foramen ovale (PFO) may be closed out of concern for ______, while ASDs are generally closed due to excessive volume loading of the ______ side of the heart. Q3: Measurement of atrial ______ oxygen saturations enables precise quantification of the severity of interatrial shunting. Q4: Oxygen saturations from multiple locations are obtained during a diagnostic ______ run. Q5: A standard balloon-tipped ______ catheter is satisfactory for sampling, but a large-bore end-hole or side-hole ______ catheter performs better rapid sampling. Q6: A left-to-right shunt is suggested when an oxygen ______ or increase in oxygen content in a chamber or vessel exceeds that of a ______ compartment. Q7: A step-up in oxygen saturation at the ______ by more than 7% above the ______ saturation indicates a significant left-to-right shunt at the atrial level. Q8: Desaturation of arterial blood samples from the left-sided heart chambers and ______ suggests a right-to-left shunt. Q9: Sequential samples from the pulmonary veins, ______, left ventricle (LV), and aorta can be obtained to determine the site of the ______ shunt. Q10: The gold standard for defining which ASDs require closure is the measurement of atrial hemoglobin oxygen ______.
A1: ATRIAL SEPTAL DEFECT (ASD), PATENT FORAMEN OVALE (PFO) A2: PARADOXICAL EMBOLISM, RIGHT A3: HEMOGLOBIN A4: SATURATION A5: SWAN-GANZ-TYPE, MULTIPURPOSE A6: STEP-UP, PROXIMAL A7: PULMONARY ARTERY (PA), RIGHT ATRIUM (RA) A8: AORTA A9: LEFT ATRIUM (LA), RIGHT-TO-LEFT A10: SATURATIONS
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Q1: Mixed venous oxygen saturation can be assumed to be fully mixed ______ blood in the absence of a shunt. ***Yet, when we are calculating shunt ratio Qp/Qs, we are confirming there is a shunt and we need to assess severity by claculating the ratio, so here mixed venous is different than PA sat. Q2: If there is a left-to-right shunt, mixed venous blood is measured one chamber ______ to the step-up. Q3: In the case of an atrial septal defect, the mixed venous oxygen content is computed from the weighted average of ______ blood. Q4: The weighted average is calculated as the sum of three times the ______ vena cava plus one times the ______ vena cava. Q5: The sum is then averaged by dividing by ______. Q6: When pulmonary venous blood is not collected, PVO2 percentage saturation is assumed to be ______%. Q7: The abbreviation “PVO2” stands for ______ vein oxygen saturation. Q8: The superior vena cava contributes ______ times in the weighted average calculation. Q9: The inferior vena cava contributes ______ times in the weighted average calculation. Q10: Mixed venous oxygen saturation is important for assessing the presence and severity of ______.
A1: PULMONARY ARTERY (PA) A2: PROXIMAL A3: VENA CAVAL A4: SUPERIOR, INFERIOR A5: FOUR A6: 95 A7: PULMONARY A8: THREE A9: ONE A10: SHUNTS
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Q1: What methods are employed to measure systemic flow in shunt calculations? Q2: In the Fick method, what formula is used to calculate systemic flow? Q3: What formula is used to calculate pulmonary flow using the Fick method? Q4: What does EPB stand for in the context of shunt calculations? Q5: Normally, how does the effective pulmonary blood flow (EPB) compare to systemic blood flow? Q6: In a left-to-right shunt, how is the effective pulmonary blood flow (QEPB) related to systemic flow and shunt flow? Q7: In a right-to-left shunt, how is the effective pulmonary blood flow (QEPB) related to systemic flow and shunt flow? Q8: What is the formula to calculate shunt volume in left-to-right and right-to-left shunts? Q9: What is the term for the ratio of pulmonary to systemic flow? Q10: What Qp/Qs ratio is considered the threshold indicating that shunt closure is necessary? *** Mixed venous blood refers to the blood collected from the pulmonary artery that contains a mixture of venous blood returning from all parts of the body.
A1: Fick method or left-sided indicator dilution methods of cardiac output determination A2: Systemic flow = (Formula from Fick method; typically CO = VO2 / (CaO2 - CvO2)). in other terms Qs ( L/min ) = [O2 consumption (ml/min)] / [ arterial - mixed venous O2 content ]. Think of flow as how much stuff (like oxygen) is used up (consumed) divided by how much difference there is between incoming and outgoing concentration !! Mnemonic: "Flow Comes Down Difference". Flow = Consumption ÷ Difference The first letters (F, C, D) can help you recall the relationship. A3: Pulmonary flow = Qp = [O2 consumption] / [ pulmonary venous-pulmonary artery O2 content ] A4: Effective Pulmonary Blood Flow or QEPB = [ O2 consumption/ [pulmonary venous - mixed venous O2 content] A5: EPB is normally equal to systemic blood flow ( QEPB = systemic flow ). It assumes pulmonary venous and arterial sat are the same because there is no shunt. A6: QEPB = systemic flow + shunt flow (left-to-right) [ we are adding the shunt flow because the shunt flow is going towards the pulmonary blood] A7: QEPB = systemic flow − shunt flow (right-to-left) { we are substracting shunt flow becuase shunt flow is going away from the pulmonary blood ] A8: Shunt volume is determined using QEPB = systemic flow ± shunt flow formulas (Equations A6 and A7 ) A9: Shunt fraction. It assesses SHUNT SEVERITY. A10: A Qp/Qs ratio greater than 1.5 ** systemic flow direction is Aorta to pulmonary artery ( arterial to mixed venous ) *** pulmonary flow direction is pulonary artery to pulmonary veins **** in normal conditions, PVO2 and arterial O2 content are similar. Also, Pulmonary artery and mixed venous are same.
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Step up
Qp/Qs = Ds/Dp ( MV here is mixed venous not mitral valve like the legend says ). Mixed venous oxygen saturation can be assumed to be fully mixed pulmonary blood in the absence of a shunt. ***Yet, when we are calculating shunt ratio Qp/Qs, we are confirming there is a shunt and we need to assess shunt severity by claculating the ratio, so here mixed venous is different than PA sat., because we know there is a shunt already.
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Effective blood flow mean usually EPBF. QEPB = [ O2 consumption/ [pulmonary venous - mixed venous O2 content] EPBF is normally equal to systemic blood flow ( QEPB = systemic flow ) when there is no shunt. It assumes pulmonary venous sat and arterial sat are the same because there is no shunt. please note there is a discrepancy between the info in this slide and the text ( about shunt flow calculation ). In the slide they used Qp or Qs but in the text they used Qs for both.
HINT : EPBF stays AWAY from the atria !! that is why in the denominator we see mixed venous and pulmonary veins both measurements are OUTSIDE the atria ! Unlike in Qp where in the denominator we see PA and pulmonary venous.
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Q1: The normal LV pressure waveform has a characteristic ________ and a small impulse outflow tract gradient ( small area between LV and Ao waveforms ). Q2: Pressure tracings are most commonly acquired with electronic ________ and fluid-filled catheters. Q3: A commonly used catheter for measuring LV pressure is the 5F ________ catheter. Q4: The femoral artery sheath side arm catheter is typically sized at ________ French (F). Q5: The resonant artifact seen in pressure tracings is also called ________, fling, or ringing. It is the defletcion near the end of the LV waveform. Q6: High-fidelity pressure tracings are obtained using ________-tipped catheters that avoid fluid coupling ( see Q1 ) Q7: Femoral artery pressure is usually ________ than central aortic pressure due to resonant signal amplification. Q8: The pressure wave measured at the femoral artery is ________ in time compared to the aortic pressure wave. Q9: Resonant artifacts occur because of the physical properties of the ________ system and fluid column. Q10: Visulaized peripheral arterial pressures are normally ________ compared with central aortic pressures.
A1: anachrotic shoulder ( slow rising and delayed peak ) A2: transducers A3: pigtail A4: 6 A5: whip A6: micromanometer ( usually avoids resonnance artifacts ) A7: higher A8: delayed A9: catheter A10: higher
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Q1: The hemodynamic assessment of AS and the success of valve therapies begin with accurate transvalvular ________ and cardiac output measurements. Q2: Many clinical catheterization laboratory measurements use the ________ artery to represent aortic pressure. Q3: Due to resonance and peripheral pressure amplification, the FA systolic pressure is ________ and delayed relative to central aortic pressure. Q4: This difference in FA pressure ________ decreases the mean gradient relative to the LV ( i think they meant to say IT artifactually increase the gradient ?) Q5: Precise pressure gradients cannot be obtained in patients with peripheral vascular disease at the level of the aortic ________ or lower. Q6: For improved accuracy in measuring the LV-Ao gradient, a ________-lumen catheter or two arterial catheters are required. Q7: The FA systolic pressure is higher and ________ compared to central aortic pressure. Q8: Peripheral vascular disease at the aortic bifurcation or lower affects the accuracy of pressure gradients when using ________ pressure. Q9: A double-lumen catheter improves accuracy by allowing simultaneous measurement of ________ and aortic pressures.
A1: gradient A2: femoral artery (FA) A3: higher A4: artefactually A5: bifurcation A6: double A7: delayed A8: femoral A9: left ventricular (LV)
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Q1: What valve does blood flow through in AS? Q2: Through what kind of aortic orifice area is blood ejected in AS? Q3: What happens to energy due to resistance as blood flows through the valve? Q4: What does energy loss cause in terms of pressure and flow? Q5: What is the name of the orifice area just after the aortic valve? Q6: What process converts kinetic energy back to potential energy after the stenotic valve? Q7: Which imaging technique measures peak instantaneous gradient across the outflow tract and is therefore able to capture the phenomenon of pressure recovery? Q8: Where are catheter-based aortic pressure measurements typically taken? Q9: What two loads sum to form the global hemodynamic load on the left ventricle? Q10: What do specialized measures relate hemodynamic load to, besides arterial resistance?
A1: Aortic valve (AV) A2: Fixed reduced (anatomic) orifice area A3: Energy is lost (portion of potential energy lost) A4: Pressure drop and acceleration of flow A5: Effective orifice area A6: Pressure recovery A7: Doppler echocardiography A8: Several centimeters distal in the aorta (after pressure recovery) A9: Valvular load and arterial load A10: Impedance to flow
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See slides
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Q1: What is the stenotic orifice called in AS? Q2: What type of energy is potential energy converted into as blood passes through the stenotic orifice? Q3: What happens to pressure as blood accelerates through the stenotic orifice? Q4: What is the name of the orifice area downstream of the vena contracta? Q5: What happens to a large part of kinetic energy downstream of the vena contracta? Q6: What is the term for kinetic energy reconverted back to potential energy? Q7: What causes the global hemodynamic load on the left ventricle? Q8: What two loads sum to form the global load? Q9: How can the global load be estimated? Q10: What physiological process dissipates kinetic energy as heat?
A1: Anatomic orifice area (AOA) A2: A portion of the potential energy of the blood, namely, pressure, is converted into kinetic energy, namely, velocity, thus resulting in a pressure drop and acceleration of flow. A3: Pressure drops A4: Effective orifice area (EOA) A5: It is irreversibly dissipated as heat due to turbulence A6: Pressure recovery (PR) A7: The summation of valvular and arterial loads A8: Valvular load and arterial load A9: By calculating valvuloarterial impedance A10: Flow turbulence
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Q1: In patients with medium or large ascending aorta, what gradient can be used instead of the net mean gradient? Q2: What does AA stand for? Q3: What does ΔPmax represent? Q4: Where is the maximum transvalvular pressure gradient (ΔPmax) recorded? Q5: What does ΔPnet represent? Q6: How is ΔPnet measured? Q7: What does LVOT stand for? Q8: What does PLVOT represent? Q9: What does SBP stand for? Q10: What does Zva represent?
A1: Standard Doppler mean gradient A2: Cross-sectional area of the aorta at the sinotubular junction A3: Maximum transvalvular pressure gradient A4: At the level of the vena contracta A5: Net transvalvular pressure gradient after pressure recovery A6: Measured by catheterization A7: Left ventricular outflow tract A8: Pressure in the LVOT A9: Systolic blood pressure A10: Valvuloarterial impedance
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Q1: What is frequently used to quickly assess the LV-Ao pressure gradient? Q2: Is the peak-to-peak gradient equivalent to the mean gradient in mild and moderate stenosis? Q3: For which severity of stenosis is the peak-to-peak gradient often close to the mean gradient? Q4: What should the peak-to-peak gradient not be confused with? Q5: Why are catheter-based measurements of peak instantaneous gradient often lower than echocardiographic measurements? Q6: What type of gradient is commonly used in echocardiographic measurements? ( generated by AI not in the paragraph but it is in the picture below ) Q7: What measurement method uses the peak-to-peak LV and aortic pressure difference? Q8: Is the peak instantaneous gradient generally higher or lower than the peak-to-peak gradient? ( generated by AI not in the paragraph but makes sense ) Q9: What phenomenon affects the catheter-based measurements of pressure gradients?
A1: Peak-to-peak LV and aortic pressure difference A2: No A3: Severe stenosis A4: Peak instantaneous gradient A5: Because of pressure recovery A6: Peak instantaneous gradient A7: Catheter-based measurement A8: Higher A9: Pressure recovery
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Q1: When using FA pressure, what type of LV-Ao pressure tracings yield more accurate valve areas? Q2: What happens if FA pressure is shifted back to match the LV upstroke? Q3: What does femoral pressure overshoot reduce? Q4: For highest accuracy, where should pressures be measured relative to the AV? Q5: What type of catheter is recommended for measuring pressures above and below the AV? Q6: How many catheters may be used for the most accurate pressure measurement? Q7: In which patients is accurate pressure measurement particularly important?
A1: Unshifted LV-Ao pressure tracings A2: Femoral pressure overshoot (amplification) occurs A3: The true gradient A4: Immediately above and below the aortic valve (AV) A5: Dual-lumen catheter A6: Two catheters A7: Patients with low cardiac output or low transvalvular gradient
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Q1: What gradient reduction indicates successful TAVR implantation? Q2: What change in aortic systolic pressure suggests successful TAVR? Q3: What does the absence of newly widened pulse pressure after TAVR indicate? Q4: What waveform feature is restored after TAVR, indicated as point d in Fig. 13.18? Q5: What is the anachrotic shoulder, indicated as point a in Fig. 13.18? Q6: What may a rapidly rising LV diastolic pressure represent after TAVR? Q7: What does the aortic pulse pressure suggest about aortic insufficiency post-TAVR? Q8: Which condition is suggested by newly widened pulse pressure ( aortic pulse pressure ) after TAVR?
A1: Reduction from 80 to 0 mm Hg A2: Increase from 105 to 122 mm Hg A3: Absence of aortic insufficiency A4: Restoration of the dicrotic notch A5: Restoration of the anachrotic shoulder A6: Unmasked diastolic dysfunction A7: Minimal or no aortic insufficiency A8: Aortic insufficiency
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Q1: What pressure is elevated in typical aortic insufficiency hemodynamics? Q2: What happens to the aortic pulse pressure in aortic insufficiency? Q3: What pressure values nearly equalize in aortic insufficiency? Q4: What might some patients require depending on valve leaflet or aortic root disruption? Q5: What condition is shown in Fig. 13.20? Q6: What gradient is noted in mixed aortic stenosis and regurgitation? Q7: What happens to the LV diastolic filling slope in mixed AS and regurgitation? Q8: What pressure nearly equilibrates with LVEDP in mixed AS and regurgitation? Q9: What does Fig. 13.21 illustrate following a TAVR procedure? Q10: What increases in the hemodynamics of a paravalvular leak post-TAVR?
A1: Left ventricular end-diastolic pressure (LVEDP) A2: It widens A3: LV and aortic end-diastolic pressures ( AO-LVEDP gradient becomes smaller ) A4: Urgent valve replacement A5: Mixed aortic stenosis and regurgitation A6: LV-Ao gradient A7: Rapid increase in slope A8: Aortic diastolic pressure A9: Hemodynamics of paravalvular leak A10: LVEDP and slope of diastolic pressure rise
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Q1: How are stenotic valve areas calculated? Q2: What two methods are used to measure cardiac output? Q3: What does the Fick calculation use to estimate oxygen consumption? Q4: What is the assumed oxygen consumption value used in the Fick calculation (mL/kg)? Q5: What is the assumed oxygen consumption value used in the Fick calculation (mL/min/m²)? Q6: What provides the best accuracy for oxygen consumption in the Fick calculation? Q7: What device is used for direct oxygen consumption measurement? Q8: What physiological parameter is essential for calculating valve areas? Q9: Is thermodilution a direct or indirect method of measuring cardiac output? Q10: Why might direct oxygen consumption measurement be preferred?
A1: From pressure tracings and cardiac output A2: Thermodilution and Fick calculation A3: Assumed consumption ( 3 mL/kg O2 or 125 mL/min/m2) or direct oxygen consumption ( metabolic oximeter ) A4: 3 mL/kg O2 A5: 125 mL/min/m² A6: Direct oxygen consumption A7: Metabolic oximeter A8: Cardiac output A9: Indirect A10: For best accuracy
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Gorlin Formula for Valve Area Valve Area =[ CO in ml/min ] / [HR × SEP × 44.3 × square root of ΔP] OR Valve Area = [ valve flow in ml/s measured during diastolic or systolic flow period ] / [ 44.3 x C x square root of MVG ] Where: CO = Cardiac Output (mL/min) HR = Heart Rate (beats/min) SEP = Systolic Ejection Period (seconds per beat) ΔP = Mean pressure gradient across the valve (mm Hg) or MPG 44.3 = A constant incorporating unit conversions and empirical factors C is an empirical constant that is 1 for semilunar valves and tricuspid valves and 0.85 for MVs,
The formula relates the flow through the valve (cardiac output) to the pressure gradient across it, allowing estimation of the effective valve orifice area. It assumes a fixed relationship between flow and pressure gradient based on fluid dynamics principles. It is widely used to assess the severity of valve stenosis, especially aortic stenosis. For AV flow, the systolic ejection period (SEP) is used: AVA= CO in ml/min / [systolic ejection period x HR ] For MV , diastolic filling period is used. MVA = CO in ml/min / [ DFPx HR ]
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A simplified formula (also known as the Hakke formula ) can provide a quick in-laboratory determination of AV area, estimated as: quick valve area = CO/ square root of peak to peak gradient For example, peak-to-peak gradient = 65 mm Hg, CO = 5 L/min, then : quick valve area = 5 l/min / square root of 65 = 5/8 = 0.63 cm2
The quick formula differs from the Gorlin formula by 18% ± 13% in patients with bradycardia (<65 beats/min) or tachycardia (>100 beats/min). The Gorlin equation overestimates the severity of valve stenosis in low-flow states.
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A continuing dilemma exists in patients with low cardiac output and small aortic-LV gradients (eg, the patient with dyspnea, poor LV function, and a 20-mm-Hg aortic-LV gradient with cardiac output of 3 L/min; AV area = 0.7 cm2).
Should this valve be replaced with a prosthetic valve that has an intrinsic gradient of 10 to 20 mm Hg? Because the Gorlin formula for AV area calculations uses an empiric constant (K) the true valve area may be variable under low-flow conditions.
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Q1: What test is necessary to distinguish low-gradient/low-flow AS causes ( cardiomyopathy vs. true stenosis ) ? Q2: What medication is used in the challenge to increase cardiac output? Q3: What was the initial LV-Ao gradient in the example patient? Q4: What was the initial cardiac output in the example? Q5: What was the initial calculated aortic valve area (AVA)? Q6: At what doses was dobutamine infused in the example? Q7: What happened to the LV-Ao gradient after dobutamine infusion? Q8: How did the cardiac output change after dobutamine infusion? Q9: Did the aortic valve area change significantly after dobutamine infusion? Q10: According to the Gorlin formula, how does mean gradient behave at low transvalvular flows?
A1: Dobutamine challenge A2: Dobutamine A3: 30 mm Hg A4: 3.2 L/min A5: 0.7 cm² A6: 10 µg/min and 20 µg/min A7: Increased to 50 mm Hg A8: Increased to 4.2 L/min A9: No, it remained fixed at 0.6 cm² A10: Mean gradient is low at all valve areas
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Q1: What is the baseline flow in the hypothetical patient? Q2: What is the baseline mean gradient? Q3: What is the baseline calculated aortic valve area (AVA)? Q4: In scenario dob 1, what does the flow increase to? Q5: In scenario dob 1, what does the mean gradient increase to? Q6: In scenario dob 1, what happens to the AVA? Q7: What does scenario dob 1 indicate about the AS? Q8: In the second scenario, what does the flow increase to? Q9: In the second scenario, what happens to the AVA? Q10: What condition does the second scenario suggest?
A1: 150 mL/s A2: 23 mm Hg A3: 0.7 cm² A4: 225 mL/s A5: 52 mm Hg A6: Remains 0.7 cm² A7: Fixed aortic stenosis A8: 275 mL/s A9: Increases to 1.0 cm² A10: Relative or pseudo-aortic stenosis
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seems to me the whole paragraph discussing patients with low LVF. I do not think there is mention for slow flow normal LVF entity.
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Hypertrophic Obstructive Cardiomyopathy
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Available catheters