Lecture 4 Flashcards
Exam 1 content
Give an example of a mixed vasodilator…
nitric oxide donors like sodium nitroprusside
What is important about the effects of mixed vasodilators on CO/VR diagrams?
The filling pressure is reduced (d/t dilation of the veins) and SVR is reduced (increased slope). The change to filling pressure is the more impactful thus CO decreases.
What is the primary action of ACE inhibitors?
afterload reducers
What are the two arteriole vasodilators we talked about in class?
- ACE inhibitors
- Hydralazine
What is the MOA of hydralazine and why do we not use it as often?
Unknown. We don’t use it as often because it takes time to work (10-15min).
How does Phenylephrine work and what is the dominant action
It is a mixed vasoconstrictor. It constricts the arterioles and the veins (increases preload). CO is near normal, but still a little lower because less blood gets to the venous system d/t increased SVR.
What is a risk of too many catecholamines circulating the body?
over time can increase risk of arrhythmias
End diastolic volume is a function of______.
preload (the atrial pressure at the end of filling or the end of phase I)
What is a good measurement for afterload?
The diastolic pressure (the pressure at the end of phase II)
if contractility increases the slope of the line is________
more steep
if contractility decreases the slope of the line is________
less steep
What happens to SV with increased preload?
increased SV d/t an increase in EDV
What happens to SV with a decreased preload?
EDV is decreased d/t less filling which would decrease SV
What happens to SV with increased afterload?
the end diastolic pressure is higher, so phase II will take longer to exceed the pressure to open the aortic valve. This will lead to a shorter phase III, less blood ejected and a higher ESV which would decrease SV if EDV remains the same
What happens to SV if afterload is decreased?
phase III will be longer, more blood gets ejected, therefore the SV is greater (and ESV is lower)
What happens if we increase contractility, but afterload and preload are held constant? What happens to CO and BP?
increased SV, EDV is normal and ESV is lower than normal. CO and BP increase
What happens to SV if we reduce contractility? What happens to CO and BP?
less squeeze, lower SV. CO and BP also decrease
Your patient had a previous MI and cardiac remodeling that has led to decreased contractility. What would happen to SV, ESV and HR? What would you use to treat them?
lower SV, higher ESV, increased HR (at first). An afterload reducer.
What is the most common valve problem we have?
Aortic valve stenosis
What would you expect SV to be in someone who has aortic valve stenosis?
SV is reduced
What is a hallmark characteristic of aortic stenosis? Why?
pulse pressure is narrowed. High pressures in the ventricle and lower pressures on the other side of the stenotic valve
What would you expect to see with mitral stenosis?
you would have filling problems. EDV is lower and SV is reduced. This would lead to an elevated preload (RAP) and increased filling pressure
what can untreated mitral stenosis lead to?
pulmonary hypertension and eventually pulmonary edema (impaired gas exchange)
What would you expect to see with aortic valve insufficiency?
retrograde blood movement. Isovolumetric periods are less defined. EDV is higher than normal and the ventricle will get stretched out
Where would you expect pressures in the ventricles exceed the atrial pressures and what would happen in response to mitral regurgitation?
Ventricular pressures > atrial pressures in phase II, III, IV. Blood leaking back into the atria especially when there is a greater pressure gradient (at the end of phase II and the beginning of phase IV)
Give some examples of things that would cause a reduction in metabolic needs and lead to a decreased CO…
Hypothyroidism
Removal of arms and legs
Give some examples of things that would increase metabolic needs and correspond to a higher CO…
Paget’s disease (excess bone), pulmonary diseases, anemia, hyperthyroidism, av shunts, BeriBeri (vitamin B1 deficiency)