Hemodynamics Flashcards
Right Atrial Waveforms
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)
Left Atrial Waveform
Same as right atrial waveform except a-wave and v-wave are larger because of lower compliance of right atrium
PCWP
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.
Increase in A-wave pressure
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
V-wave
- affected by amount of blood filling atrium during systole
- MR can cause giant V-waves as LA filled via PV and LV (backwards)
Starling curve
SV y-axis, preload x-axis
shift curve up by increasing contractility or decreasing afterload
shift up along line by increasing preload
Force tension curve
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)
PV loop
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)
Phenylephrine
Pure Alpha AGONIST - increases afterload (no effect on preload, contractility)
Isoproterenol
B1 Agonist (increases contractility) B2 Agonist (decreases afterload - vasodilates) Good to ellicit dynamic LVOT obstruction in HOCM patients
Norepinephrine
90% Alpha agonist (increases afterload - vasoconstrictts)
10% B1 Agonist (contractility increase)
Epinephrine
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»_space;B2 agonist so INCREASES afterload
Phentolamine
Alpha ANTAgonist - decreases afterload
Prazosin
Selective alpha 1 antagonist only (no blocking of alpha 2 which also decreases release of alpha 1)
Propranolol
B1 (inc contractility) antagonist, B2 antagonist (increase afterload)