Cardio-physio-cardiac output-slivkoff Flashcards
What 3 determinants of stroke volume?
afterload, preload, and contractility
Stroke volume X HR =
cardiac output
Afterload has a positive/negative affect on stroke volume?
negative
Preload and contractility have what kind of effect on stroke volume?
positive, as either increase, stroke volume increases
What is preload?
filling pressure
What is afterload?
arterial pressure opposing ejection
As more venous return enters the heart, the cardiac output increases. This process describes increased preload or afterload?
Preload
The more blood you give the heart, the more/less it is going to pump out
more
There is an ideal length that maximizes the overlap between actin and myosin and maximizes generated.
tension
What are some ways to change the number of crossbridges being made in the sarcomere?
- alter preload (either more or less)
- more Ca2+
According to the Frank-Starling Mechanism diagram, as stroke volume increases, ventricular end diastolic volume .
inceases, but it can platuea and decrease if there is too much of either
What 4 main factors can change preload?
- increase in blood volume (increase preload)
- venoconstriction (increase preload)
- skeletal muscle pump (increase preload)
- nitroprusside (venodilation) -decrease preload
How does inspiration and expiration change preload?
inspiration increases preload
expiration decreases preload
What are the main funcitons of ACE inhibitors and angiotensin II receptor blockers?
the decrease overall blood volume which in turn decreases BP
What kind of effect does tricuspid and mitral valve stenosis have on stroke volume?
decreases stroke volume by decreasing preload and ventricular outflow
What kind of effect does aortic stenosis have on preload or stroke volume?
Aortic stenosis would increase diastolic ventricular pressure and lead to decreased ventricular filling, leading to decreased preload and stroke volume
What kind of effect does atrial tachycardia have on stroke volume?
It would lead to a fib and decreased ventricular filling time, which would not leave enough time to fill up ventricle
Changing from an upright to supine position does what to preload?
It increases preload as there is less blood pooling in lower parts of body
What term describes the arterial pressure right after the aortic valve (pressure through all the major arteries)?
afterload
High BP is an increase/decrease in afterload (arterial pressure opposing ejection)?
increase
Increasing total peripheral resistance (TPR) would have what effect on afterload?
Increase afterload and BP
How does decrease of systemic vascular resistance affect afterload and stroke volume?
It woud decrease afterload and therefore increase SV
What effect does hydralazine, ACE inhibitiors, angiotensin II receptor blockers, have on SV and afterload?
They are all vasodilators, would decrease BP, which would decrease afterload and increase SV
Exercise causes an increase/decrease in vascular resistance?
decrease in vascular resistence, which would increase stroke volume and decrease afterload
Decreased pulmonary resistance caused by phosphodiesterase inhibitors (vasodilator) would have what effect on the right ventricle?
Decrease afterload and increase SV to right ventricle
What does increased systemic and or peripheral vascular resistance (chronic HTN and vasopressors) and aortic valve stenosis do to afterload and SV?
Increase afterload and decrease SV
What is another way to describe wall stress?
afterload
Wall stress increases/decreases with increased ventricular pressure (HTN) and increase ventricular radius (dilated cardiomyopathy)?
increases
Wall stress increases/decreases with increased ventricular thickness (hypertrophy)?
decreases (more myocytes taking on stress, reduces the stress felt by each myocyte)
dP/dt (pressure/time) could be a measure of what?
contractility (steeper line means more contractility)
How to calculation ejection fraction?
Stroke volume/ end diastolive volume
What do catecholamines and positive inotropes (digoxin) do to heart contractility?
increases contractility
What does loss of myocardium, B-blockers, non-dihydropyridin Ca2+ channel blockers, and dilated cardiomyopathy do to contractility?
Decreases contractility
What effect does decreased extracellular Na+ (due to decreased Na+/Ca2+ exchanger activity) have on contractility?
Increases contractility as there is more Ca2+ left in the heart
What effect does digitalis have on contractility?
It inhibits the Na+/K+ pump, which decreases the intracellular Na+, which decreases activity of the Na+/Ca2+ exchanger, leading to increase Ca2+ in the heart and increased contractility
What is the effect of thyroid hormones on contractility?
Increases contractility (by making more B1 adrenergic receptors)
What effec do B1-receptor blockers have on contractility?
decreases contractility
What effect does hypoxia have on contractility?
Decreases it
What do narcotic overdose, hypercapnia (increased CO2), hyperkalemia, and acidosis have in common as concerning contractility?
they decrease contractility
What effect does increase venous tone have on preload?
contraciton of venous vessels enhances venous return and preload
As blood moves through the heart, increased arterial constriction would lead to increased/decreased peripheral resistance, which would increase/decrease stoke volume?
increased peripheral resistance; decreased stroke volume
Arterial vasodilation/ vasoconstriction leads to increased SV and CO?
vasodilation (less pressure for the heart to fight against)
Venous vasodilation/venoconstriction leads to decreased SV and CO?
vasodilation (as there is less oompf of the blood entering the heart)
More blood volume (venous return) and increased venous tone (activated by SNS) does what to preload?
Increases preload
What does an increase ventricular radius and ventriclar pressure do to afterload according to LaPlace’s law (wall stress = increased afterload)?
increases afterload, decreasing SV and CO
According to LaPlace’s law, how does increased ventricular thickness affect wall stress, and therefore afterload?
Ventricular thickness decreases wall stress (shared load by more myocytes) and decreases afterload
What is the product of CO and systemic vascular resistance?
Blood pressure
What do SNS a1 receptors, angiotensin II, endothelin, and O2 have in common?
They decrease arteriolar diameter, vasoconstriction
What do B2 receptors, NO, adenosisn, decreased pH, and prostaglandins have in common?
They increase arteriolar diameter, leading to vasodilation
What is the pressure that is measured when the heart has stopped?
Mean circulatory filling pressure or mean systemic pressure
Cardiac output will always match .
venous return
Given the same contractility, if you increase volume into the system (IV), what happens to the mean circulatory filling pressure (when heart is stopped)?
The mean circulatory filling pressure will increase, which will result in an increase in CO or venous return?
which way does the vascular funtion curve shift with increased blood volume?
It shifts the curve up
which way does the vascular funtion curve shift with decreased blood volume?
It shifts the curve down
If we increase contractility, what type of effect will occur with the cardiac function curve?
The curves shifts upward
If we decrease contractility, what type of effect will occur with the cardiac function curve?
The curve shifts down.
What happens to the curves during increased total peripheral resistance (TPR or vasoconstriction)?
The cardiac funtion curve and vascular function curve shift down but the pivot point stays the same.
What happens to the curves during decreased total peripheral resistance (TPR or vasodilation)?
They both increase but the pivot point stays the same.
Review diagram
What happens to the pressure volume loop with excercise?
SV increases, EDV increases, contractility increases, decrease in afterload. ( We have not added more blood but squeezed out the blood in the veins with the skeletal muscle pumps).
Review diagram
