hemodynamics Flashcards

1
Q

stroke volume (SV)

A

volume ejected from the ventricles with each systolic contraction aroudn 70mls/ beat

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2
Q

cardiac output (CO)

A

SV x HR

normal around 5L-6L in males

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3
Q

what is cardiac index

A
used to normalize CO across population by accounting for size 
CI= CO/ BSA
BSA (body surface area)
normal value
 2.6-4.2L/min/m2
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4
Q

wide range of HR

A

HR has the widest range of variability potential increases of 100-200%
SV can only increase 50%
this means that as HR increases filling time decreases and so CO is reduced,
this is seen with shock and abnormal rhythms

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5
Q

preload (SV)

A

preload is the final stretching of the cardiac myocytes prior to contraction. stretch is the lengthening of sarcomeres at end diastole

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6
Q

how is preload measure ?

A

cannot be measure directly so end diastolic volume (EDV) or end diastolic pressure (EDP) is used as a proxy.

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7
Q

what does an increase in stretch within physiological limits do to the ventricle ?

A

the greater the stretch= stronger contraction

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8
Q

what does the frank starling and venous return chart explains ?

A

the greater the stroke volume (more blood-max stretch ) the greater the contraction therefore it increases the blood venous return

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9
Q

factors that can increase ventricular preload

A
  • increase venous pressure 9decrease compliance or increase venous blood volume)
  • increase ventricular compliance
  • increase atrial inotropy (strength of contraction)
  • increase outflow resistance and afterload
  • decrease HR
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10
Q

what is Afterload

A

afterload is the “load” against which the heart must contract to eject blood
under normal circumstances the greatest contributor to afterload pressure is aortic pressure

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11
Q

afterload and stroke volume

A

an increase in SV= decrease in afterload

a decrease in SV= increase in afterload

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12
Q

what does inotropy mean ?

A

Force of contraction or “Contractility” can be influenced independently from preload and afterload on a cellular level.

“Changes in inotropy are caused by cellular mechanisms that regulate the interaction between actin and myosin independent of sarcomere length”

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13
Q

inotropy on stroke volume

A

increase in Inotropy= increase SV

reverse with a decrease in inotropy

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14
Q

factors influencing inotropy

A
  • ↑ sympathetic activation
  • ↑ circulating catecholamines (adrenile)
  • ↑ afterload (anrep effect)
  • ↑ heart rate (bowditch effect)
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15
Q

what is the anrep Effect ?

A

The Anrep effect is an autoregulation method in which myocardial contractility increases with afterload.
the hear is gonna squeeze harder with an increase afterload, compensatory effect in order to overcome resistance.

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16
Q

what is the bowditch effect ?

A

an autoregulation method by which myocardial tension increases with an increase in heart rate.
inotropy increases as your heart rate increases, to compensate for the loss of filling time

17
Q

positives inotropes

A
increases inotropes
digoxin 
beta antagonist 
-dopamine 
-dobutamine 
-epinephrine 
-isoproterenol
phosphodiesterase inhibitors 
-milrinone
18
Q

negative inotropes

A
parasympatheric stimulation- vagus nerve (decreases heart rate) 
hypoxia
acidosis 
anesthesia 
increased potassium 
calcium channel blockers
19
Q

three methods to measure CO

A

ficks method
thermal dilution
dye dilution

20
Q

what is the ficks method concept

A

is the rearrange of the uptake of a oxygen this can determine on the factors of blood flow and the arterua venous contenc difference
VO2/ C(a-v)O2

21
Q

dye dilution method

A

makes use of phot spectrometry to analyze the concentration of dye over time .

22
Q

thermal dilution method

A

A Pulmonary Artery Catheter is inserted into a central vein
The proximal port lies in the right atrium
A known volume with a known temperature is injected
Eg. 10 cc of 0 degrees celcius
The end of the catheter has a temperature probe
This distal end is set to lie in the Pulmonary Artery
The RV functions as a mixing chamber