Heart Failure Pressure Volume loops/Pharm Flashcards
What drugs are used for chronic heart failure?
- Diuretics (furosemide, chlorothiazide, triampterene)
- Drugs tht target the renin-angiotensin-aldosterone axis
- ACE inhibitors: captopril, enalapril, lisinopril
- Angiotensin receptor blockers: losartan, valsartan, valsartan/sacibitril combination
- Aldosterone antagonists: spironolactone, eplerenone
- Vasodilators: hydralazine, Isorbide dinitrate
- B- Adrenergic receptor blockers: metoprolol, carvedilol
- Heart rate reducing agents: Ivabradine (blocks If current)
- Positive inotropic agents: DIgoxin
What drugs are for Acute HF?
Loop Diuretics: Furosemide
Vasodilators: Nitroglycerin, nitroprusside
POsitive inotropic agents: Dobutamine, dopamine, milrinone
Normally Cardiac output is matched to _______-
What is the equation for cardiac output
3 major determinants of stroke volume:
Normally cardiac output is matched to metabolic needs
CO= HR * SV
3 major determinants of stroke volumeL contractility, preload, afterload
WHat is preload?
the more a normal ventricle is distended (filled with blood) during diastole, the greater the amount of blood ejected during the next contraction (Frank-Starling, cardiac function increases as a function of preload)
preload measured as end diastolic volume or pressure (indicates the degree of myocardial stretch at the end of diastole
What is afterload?
resistance the ventricle must overcome to empty its contents (ventricular wall stress that develops during systolic ejection. estimated by LaPlace)
rises in response to higher pressure load (HTN) or increased chamber size (dilated LV)
increases in wall thickness serves a compensatory role to reduce wall stress
What is contractility? How is a change in contractility visualized on a Frank-Staling curve?
accounts for changes in myocardial force for a given set of preload and afterload conditions (dependent on chemical and hormonal influences)
On a Frank-Starling Curve a change in contractility shifts the curve upward or downward in direction
What is:
a
a-b
b
b-c
c
c-d
d
d-a
green dot
blue dot
arrow in the center
a: mitral valve opening
a-b: diastolic filling
b: mitral valve closing
b-c: isovolumetric contraction
c: aortic valve opening
c-d: ejection
d: aortic valve closure
d-a: isovolumetric relaxation
green dot:
blue dot:
arrow in the center: SV= EDV-ESV
What is changing in this pressure-volume loop?
preload (the EDV is increasing)
SO you can see that this leads to an increased SV.
SV=EDV-ESV
How is a pressure volume loop influenced if the compliance is reduced?
This means that the heart is stiffer
This leads to an increased slop of the pressure volume line. SO you get the same EDV you need higher pressure bc the heart is difficult to fill (it won’t stretch)
OR if you use the same pressure you get a lower EDV.
What is chnaging in this pressure volume loop?
Afterload! (the amt of pressure the heart has to overcome during ejection.)
Relationship between ESV and afterload is approximately linear (End Systolic pressure-colume relationship ESVPR). The greater the afterload the higher the ESV (bc you can’t push all of the blood out)
SV is decreased
What is changing in this pressure-volume loop?
Contractility!
The slope of the ESVPR line is a function of contractility
with increased contractility the line becomes steeper, hence the ventricle empties more completely resulting in a smaller end-systolic volume this increased SV
Increased contractility= Increased SV, and decreased ESV
SV is a function of ____, _____, and _____
End-Diastolic VOlume (or EDP) is used as an index of ______
End-systolic volume depends on the ____ and _____ but not on _______
- SV is a function of preload, afteload, and contractility
- Increased with increased preload, decreased afterload or increased contractility
- EDV (or EDP) is used as an index of preload
- EDV is influenced by chamber compliance. as compliance increases EDV decreases (if presure is cnstant) increases the slope of the volume/pressure line
- ESV depends on afterload and contractility, but not on preload
Heart Failure is a result of a wide variety of CV diseases, those that: ________, _______, and __________
Heart failure can be due to abnormal ________ and/or ________
Patients are categorized according to ________
- Heart failure is a result of CA diseases that
- impaire ventricular contractility
- increase afterload
- impair relaxation and filling
- Heart failure due to abnormal
- emptying (ie systolic dysfunction)
- filling (ie diastolic dysfunction)
- Patients categorized according to ejection fraction (EF)
- Heart failure with reduced EF
- Heart failure with reserved EF
What is the difference between SV and EF?
SV is the absolute volume of blood that is ejected from the heart
EF is the fraction or percentage of total blood that is ejected when the heart contracts
SO: if EF is 50% and the heart fills 100ml then SV will be 50ml. But if EF is 50% and heart only fills 80ml (maybe due to decreased compliance) then the SV will be 40ml.
In Heart failure with reduced ejection fraction why does the ventricle have diminshed capacity to eject blood? What might this result from?
- Ventricle has diminshed capacity to eject blood because of impaired contractility or pressure overload
- loss of contractility may result from:
- destruction of myocytes
- abnormal myocyte function
- fibrosis
- With pressure overload, ejection is impaired by increased resistance to outflow
In heart failure with preserved EF what is usually abnormal? WHat are some examples?
Heart failure with preserved EF usually demonstrates abnormalities in diastolic function- impaired early relaxation and/or increased wall stiffness
For instance: actue ischemia
hypertrphy
fibrosis
restrictive cardiomyopathy
pericardial diseases
**EF is preserved, but SV is decreased bc the heart doesn’t fill well
How does the Frank-Starling mechanism compensate in heart failure?
there is limited benefit
with severly depressed contractile function, curve may be falt at higher diastolic volumes reducing augmentation of increased chamber filling
increased filling pressure amy result in pulmonary congestion and edema
**so basically a healthy heart, when you increase pre-load the CO will increase significantly. In heart failure the contractility is decreased so the slope of the line is flatter. therefore an increase in pre-load doesn’t significanty increase SV and CO.
How is neurohormonal activation a compensatory mechanism in heart failrue?
serves to increase peripheral vascular resistance, which maintains perfusion of vital organs during reduced cardiac output
also promotoes water and sodium retention, which increases intravascular volume and preload, which maximizes cardiac output via the Frank-Starling mechanism
Although this is initially beneficial, continues activation ultimately proves harmful
What are the 3 neurohormonal repsonses to decreased cardiac output and what do they lead to?
- Increased sympathic nervous system
- increase contractility
- increase SV
- increase HR
- increase CO
- vasocsonstrict (arteriolar)
- maintains BP, but decreases CO
- vasoconstrict (venous)
- increases venous return to heart, increase preload
- increase contractility
- Increases Renin-Angiotensin system
- vasoconstriction (arteriolar)
- maintains blood pressure but decreases CO
- vasoconstriction (venous)
- increases venous return to the heart and increases preload
- increases circulating volume (retain salt and water)
- increases venous return to heart and increases preload
- vasoconstriction (arteriolar)
- Increase Antidiuretic Hormone
- increase circulating volume
- increases venous return to heart and increase preload
- increase circulating volume
