Applied Physiology: CV Barash Flashcards

Question

RV vs LV afterload systems?

Answer 1

Systemic Circulation less compliant than Pulmonary arterial vasculature... so LV less compliant??? (Look into more) LV is less sensitive to changes in afterload than RV??? (Look into more)

Answer 2

1) Aortic input impedance ... the ratio of continuous aortic pressure to blood flow Measured by Power Spectral or Fourier series analysis (limited practical application) 2) Quantification of the mechanical forces to which the LV is exposed at the end of ejection - LV end-systolic wall stress

Answer 3

Changes in elevated pressures and wall thickness means increase in LV End-Systolic Wall stress ... maximum at early LBV ejection and then falls This increase in LC systolic wall stress is a stimulus for myocye hypertrophy when chronic increases afterload are present (chronic aortic stenosis or uncontrolled essential hypertension)

Answer 4

Yes At end systole, forces driving further ejection and those resisting it are equal (LOOK INTO MORE!!??)

Answer 5

Afterload looked at from a mechanical system perspective LV and arterial vasculature must match appropriately to assure optimal energy transfer between them LV and arterial circulation are considered elastic chambers in series ... thus LV-arterial coupling = Ees (LV elastance): Ea (effective arterial elastance Ea = ratio of end-systolic arterial pressure to stroke volume (which could be applied to ~LV afterload... not all the time because lacks arterial frequency dependence or wave refleciton properties) ... arteriolar resistance and compliance of proximal great vessels influence it (LOOK INTO MORE) Barash pg.291

Answer 6

Systemic Vascular Resistance (refkects resistance of terminal arterioles) ([MAP-RAP]x80)/CO MAP = Mean arterial pressure (can determine from BP) RAP = Right atrial pressure CO = Cardiac Output (SVxHR)

Answer 7

Mechanical properties of the blood and arterial walls Frequency -dependence if arterial pressure and blood flow Arterial wave reflection ... all important in elderly and those with atherosclerosis BEST used as a nonparamatic estimate, not quantative index, of LV produced by vasoactive medications or CV disease

Answer 8

Increases in afterload Adaptations then ensue: ... SNS tries to improve contractility to compensate, but this response causes unintentional, but equally important increases in LV afterload that often negates the expected increase in CO from the improved contractility ... LV hypertrophy to chronic increases in LV afterload, that reduces LV wall stress by increasing wall thickness, BUT increases O2 demand and reduces LV compliance... make the hypertrophies LV more susceptible to myocardial ischemia and diastolic dysfunction TRULY WANT TO DECREASE LV AFTERLOAD BY REDUCING THE INCITING STRESS IN A FAILING HEART

Answer 9

Force that cardiac muscle is capabale of producing during contraction under controlled loading conditionins and stimultion rate. Finding the gold standard is elusive... LV P-V analysis, isovolumetric contraction and ejection are the major ways to measure it... but with limitations

Answer 10

Very close to the upper left corner The Emaxs' of different loading conditions create the ESPVR slope (End-systolic elastance; Ees) - thus it is an afterload sensitive index of contractility because of how it is taken at end-systole Barash pg 202

Answer 11

Increases Ees and the magnitude of this increase quantifies the positive intoropic effect of the drug Barash pg 202

Answer 12

LV Contractility Keep in mind that profound EF depression in a patient with severe hypertension may occur because afterload is markefly increased, not because myocardial contractility is grossly impaired... or inaccurate due to mitral and/or aortic valve disease or ventricular septal defect In the presence of an atrial regurg, EF could be higher because blood is going back into the atria as well... not because the heart is "hyper dynamic"

Answer 13

A reduction in LV Ejection Fraction HFNEF = Heart Failure with Normal Ejection Fraction (major cause is LV diastolic dysfunction)

Answer 14

Loading conditions as many VA and IV anesthetics affect LV relaxation and filling in the normal and failing heart

Answer 15

Tissue relaxation Abnormality in the process delays relaxation If LV is delayed in relaxation, early LV filling is effected and thus becomes more dependent on atrial systole... which can then lead to A-fib Myocardial ischemia, which is frequently accompied by reductions in LV compliance, limit LV filling... thus leading to LA and pulmonary venous hypertension and thus pulmonary edema

Answer 16

Measuring rate at which LV pressure declines during isovolumetric relaxation

Answer 17

Not only augment LV systolic function but also simultaneously enhance LV relaxation (decrease T) in patients with heart failure. Which helps improve early LV filling dynamics and reduce congestive signs and symptoms

Answer 18

Need higher LV pressure to distend it to a given volume Cardiac tamponade is an exception. Modulus of chamber stiffness if "normal" (K would be constant), even though LV pressure is greater at each LV volume - parallel shift in the EDPVR (up and to the left) ... thus position of EDPVR might be more important than K

Answer 19

IVRT Duration between aortic valve closure (end-systole) and mitral valve opening (onset of transmitral blood flow) Noninvasive index of LV relaxation measured in M-mode or pulse wave on Doppler echocardiogrpahy Barash pg 295

Answer 20

Transmitral blood flow velocit Venous blood flow velocity pattern ... many times used together to quantify LV diastolic dysfunction

Answer 21

LA relaxation = stimulates forward movement of blood through pulmonary veins Mitral valve annulus moves towards LV apex = helps draw more blood from pulmonary veins into LA (engine piston) Mitral valve opens = blood stored flows into LV, letting more blood from Pulmonary Veins to flow into LA In elderly, as LV diastolic dysfunction worsens, LA must compensate to fill it up

Answer 22

Intrathoracic pressure declines during inspiration, increases venous return to right side of heart, dilates RV, pushes on LV thus limiting its filling causing a small decrease in SV and MAP During expiration, it is reveresed Pericardial tamponade or constrictive pericarditis exaggerates this effect ... be aware cardiovascular collapse is possible with initiation of PPV due to this decreased venous return on "inhalation", counter to what the body is used to

Answer 23

Emptying Fraction Dependent on LA contractility, preload, and LV Compliance

Answer 24

Chronically elevated because of severe LV diastolic dysfunction or mitral regurg Could limit its ability to contribute to EDV as contractile chamber

Answer 25

LV compliance and pressure during late diastole LV Diastolic dysfunction = increased work for LA LA (like the RV) is more susceptible to acute increases in afterload than LV due to less muscle mass and thinner walls LA Emptying Fraction will initially increase during LV diastolic dysfunction, but then decrease as LA contractile dysfunction develops with chamber dilation... will eventually cause remodeling and thus reduced compliance in LA, furthering limiting venous pulmonary return

Answer 26

Compensatory LA Emptying Fraction increases Passive LA EF declines

Applied Physiology: CV Barash Flashcards

(50 cards)