Hemodynamics

Question 1

Right Atrial Waveforms

Answer 1

a wave - first positive deflection - atrium contraction - p-wave on ecg
c-wave - 2nd deflection - during RV contraction when TV is closed TV bulges into RA and causes this deflection (right after QRS on ECG)
X descent - depolarization of right atrium and TV ring is being pulled into RV (between QRS and T wave)
V-wave - passive filling of RA when TV is closed (twave)
Y-descent - rapid fall in RA pressure as TV opens and RA is emptied into RV during ventricular diastole (after t-wave on ECG)

Question 2

Left Atrial Waveform

Answer 2

Same as right atrial waveform except a-wave and v-wave are larger because of lower compliance of right atrium

Question 3

PCWP

Answer 3

Same as LA waveform except dampened and and shifted to right (delayed) in relation to LA waveform since pressures need to travel through pulmonary veins, capillaries and arteries before reaching transducer.

Question 4

Increase in A-wave pressure

Answer 4

Conditions that cause high atrial pressures

• MS/TS
• decreased compliance of atrial walls (ie constrictive pericarditis, tamponade
• NO a-wave with afib
• MR/TR can also increase A-wave as increased blood volume flowing through atrium
• decreased a-wave during hypovolemia

Question 5

V-wave

Answer 5

• affected by amount of blood filling atrium during systole

- MR can cause giant V-waves as LA filled via PV and LV (backwards)

Question 6

Starling curve

Answer 6

SV y-axis, preload x-axis
shift curve up by increasing contractility or decreasing afterload
shift up along line by increasing preload

Question 7

Force tension curve

Answer 7

SV y-axis, afterload x-axis
shift up curve by increasing contractility or increasing preload
shift forward on curve by increasing afterload (which decreases SV)

Question 8

PV loop

Answer 8

ESV lower right corner
EDV lower left corner
AV valve opens - upper left corner
AV valve closes - upper right corner
Preload = volume at EDV - shifts inward with diuresis (dec’ing SV) and outward with vol (inc’s SV)
Afterload - just a shift along ESPVR line - Isovolumic contraction continues until LV pressure = aortic pressure (ie afterload) and AV valve opens there and ejects until it hits ESPVR line - that width is SV
End systolic pressure volume relationship = contractility line - when loop hits that line ejection stops
-shifting line up and to left = increase in contractility
Kp modulus line (at bottom) is end diastolic pressure volume relationship - pressure increases slowly as ventricle fills during diastole (steeper curve with stiffer ventricle and diastolic dysfunction)

Question 9

Phenylephrine

Answer 9

Pure Alpha AGONIST - increases afterload (no effect on preload, contractility)

Question 10

Isoproterenol

Answer 10

B1 Agonist (increases contractility)
B2 Agonist (decreases afterload - vasodilates)
Good to ellicit dynamic LVOT obstruction in HOCM patients

Question 11

Norepinephrine

Answer 11

90% Alpha agonist (increases afterload - vasoconstrictts)

10% B1 Agonist (contractility increase)

Question 12

Epinephrine

Answer 12

50% Alpha agonist (increases afterload)
50% B1 agonist (inc contractility) & B2 (decreases afterload)
Note:
Physiologic release of Epi - B2 effect > Alpha effect so decreases afterload
Ampule high dose epi - Alpha agonist&raquo_space;B2 agonist so INCREASES afterload

Question 13

Phentolamine

Answer 13

Alpha ANTAgonist - decreases afterload

Question 14

Prazosin

Answer 14

Selective alpha 1 antagonist only (no blocking of alpha 2 which also decreases release of alpha 1)

Question 15

Propranolol

Answer 15

B1 (inc contractility) antagonist, B2 antagonist (increase afterload)

Question 16

Metoprolol

Answer 16

B1 only antagonist (no B2 broncoconstriction)

Question 17

Labetolol

Answer 17

Alpha 1 antagonist (dec afterload) B1 antagonist (decreases contractility), B2 antagonist (increases afterload)
Most powerful BP drug…

Question 18

Dobutamine

Answer 18

B1 AGONIST (increases contractility) - shifts upward ESPVR line - decreasing ESV, increasing SV by increasing contractility

Question 19

Normal

Answer 19

RAP DECREASES with inpiration
inc’s Y descent
blunts X descent

Question 20

HF or constriction

Answer 20

RAP INCREASES with inspiration
despite exagerrated Y descent
=kussmal’s sign

Question 21

Valsalva

Answer 21

Normally RAP decreases on inspiration and y descent exagerrated so move together
If RAP elevates or stays same with inc’d y descent - kusmalls (HF/constriction)

Question 22

Tamponade

Answer 22

Loss of Y-descent
First A wave(atrial contraction), then another deflection up is c wave (TV elevation into RA) then continues down as X descent(downward movement of RV contraction) - next positive deflection is V-wave (filling of RA) and NEXT downward descent after V-wave is y-descent -> blunted in TAMPONADE

Question 23

Constriction

Answer 23

RAP elevated - retains X and Y descents…

Question 24

Use of Swan

Answer 24

DO NOT USE if patient normotesive and with ADHF and responding to diuretics/vasodilators as expected

Question 25

How to measure JVP

Answer 25

Clavicle upward in upright position

Question 26

Valsalva

Answer 26

Phase 1: Onset of strain, increased intrathoracic pressure, NO HR change, inc BP
Phase 2: Strain continues, dec in venous return, dec in SV and Pulse pressure - HR inc’s, BP drops
Phase 3: Release of strain - decrease in intrathoracic pressure, normalization of pulmonary blood flow
Phase 4: BP overshoot - return of HR to baseline

Question 27

Valsalva

Answer 27

Phase 1: Initial pressure rise (initiation of strain) - application of expiratory force - pressure risings inside chest forcing blood out of pulmonary circulation into LA - mild rise in SV, BP no change in HR
Phase 2: Reduced venous return and compensation (continued strain) - return of systemic blood to heart is impeded by increased pressure inside chest - CO/SV dec’d, BP down - compensatory tachycardia
Phase 3: Pressure release - pulmonary blood vessels and aorta re-expand - further fall in SV due to decreased return to LA - decreased intrathroacic pressure - venous blood can enter chest and heart - CO starts to increase
Phase 4: Return of CO - blood return to heart enhanced by release of blood that was effectively dammed back - rapid rise of CO to above normal briefly then back to baseline - with CO/BP nromalized, pulse back to baseline

Question 28

Valsalva on murmur (phase II)

Answer 28

decreases preload to heart
Decreases:
AS,
PS,
TR
Increases
HCM
MVP

Question 29

Valsalva

Answer 29

1) Inititiation of valsalva - rise in aortic pressure (intrathoracic pressure increases forcing blood out of pulm circuit into LV -> inc’s SV and BP)
2) Maintenance of valsalva - fall in pressure with tachycardia (LV filling declines, inc’d intrathoracic pressure impedes venous return, SV drops -> results in vasoconstrction and compensatory tachycardia)
3) Release of valsalva - further initial fall in BP with release of the Valsalva (decreased intrathroacic pressure, decreased LA return associated with inc’d aortic volume and delay before venous catch up with LV)
4) recovery period with bradycardia with BP overshoot as SV increases rapidly into vasoconstricted aortic system( LV preload increaes with return of venous return, SV increases rapidly against vasoconstricted aorta so BP overshoots - barorecteptos stimulated so HR falls).