Flashcards in Hemodynamics #6 Deck (16):
Make CO relative to body size
CI = CO / BSA
Normal: 2.5-4.2 LPM
Stroke volume and ejection fraction
SV - 2/3 end diastolic volume
-thus normal ejection fraction (EF) - 67%
-EF >55% is ok
How do we decrease preload?
Ace inhibitors (slow)
How is preload increased?
Monitored by CVP or PCWP
Vasoconstrictors (typically fast)
-neosynephrine (venous side)
HR x SV
Normal is 4-8 LPM
-PVR increases & decreases
Decrease with dehydration & RV failure
-increased w/ anything that causes pulmonary HTN
-Increases & decreases
-decreases w/ dehydration, distributive shock, vasodilators (Nitroprusside, low dose dopamine, nitro)
-increase w/ IHSS, HTN, vasoconstrictors, shock states.
Idiopathic Hypertrophic Subaortic Stenosis.
-fat septum - hypertrophic cardiomyopathy => fat septum will not allow aortic valve to open => LV cannot clear
Medications to decrease afterload
-Nitroprusside (nitrate donor) - nitric oxide most potent vasodilator
-fenoldopam (corlapam) - dopamine agonist / vasodilate mesenteric
-nifedipine (procardia), nicardipine (Cardene) Ca channel blockers
-dobutamine (Dobutrex) - B2 / B1 agonist
-nesirtide (natrecor) RAA inhibitor, synthetic BNP
Medications to increase afterload
-Dopamine - A1 agonist (high doses) / significant beta activity as well
-Phenylephrine (Neo-synephrine) pure A1 agonist, will not Improve pump problems.
-norepinephrine (Levophed) A1 agonist above 2 mcg/min, don't use with pump problems.
Robs preload, decreases diastolic filling time, increases myocardial oxygen demand.
Contractility increases by which actions?
-increases calcium levels (IV Ca considered especially w/ trauma)
-cardiac glycosides (digitalis)
-B1 agonists (dobutamine (#1), epinephrine)
Contractility is decreased by which mechanisms?
-primary four: potassium, Magnesium, phosphorous, calcium
-correct shock states, oxygenation, bicarbonate
#1 cause of dampened waveform (hypodynamic)
Air in the line