The heart pump Nov1 M2 Flashcards
what S1 (1st heart sound) corresponds to
closure of the AV valves (tricuspid and mitral) during systole
what S2 corresponds to
closure of seminular valves (aortic and pulmonic) at start of diastole and start of isovolumetric relaxation
seminular valves (2)
aortic and pulmonary valve
S3 corresponds to what
heart sound when ventricular filling at diastole when blood hits the ventricle wal
S3 heard where (2)
individuals with very good diastole or indiv. with heart failure
why hear S3
because vacuum created by ventricle relaxation
ventricle relaxation passive or active
active (ATP dependent). put calcium back in SR
S4 corresponds to what
atrial contraction when pumps blood in stiff ventricle (non compliant)
S4 heard where
abnormal (pathologic) in patients with non compliant ventricle
if had 4 heart sounds, in what order would hear them
S1, S2, S3, S4
pressure volume loop. how to get that
plot left ventricular pressure as a function of ventricular volume
pressure volume loop 1st part (out of 4)
mitral valve opens, ventricle fills slowly (go to right, increase in volume and slight increase in P) until EDV
pressure volume loop 2nd part
isovolumetric contraction. pressure rises but volume stays the same (vertical rise)
pressure volume loop 3rd part
aortic valve opens, ejection, ventricular volume falls to ESV. pressure rises but falls back a little
pressure volume loop 4th part
from ESV, isovolumetric relaxation. vertical drop in P without change in volume. until mitral valves open
why ventr pressure goes up when filling (increasing volume)
bc even though ventricles stretch, limited by pericardial cavity
ESPVR def
end systolic pressure-volume relationship. (P and V relationship in ventricle at end of systole)
ESPVR is an indicator of what
how strong the heart is
ESPVR: what determines the moment when systole ends
is when aortic valve closes (when P aorta = P ventricle)
EDPVR stands for what and what it does
end diastolic pressure-volume relationship. (P ventr as function of ventr. volume during filling of ventricle)
EDPVR shape
follows first part of pressure volume loop and extends a bit higher and further to the right
length-tension relationship or cardiac muscle length-tension cycle: what it is
ventricular muscle tension as a function of muscle length
what curve does cardiac muscle length-tension cycle ressemble and why
the pressure volume loop bc ventricular volume and muscle length are related linearly
how to see stroke volume on a PV loop
right vertical line minus left vertical line (EDV - ESV)
3 determinants of stroke volume
preload, afterload and contractility
preload def and effect
EDV. Greater EDV gives greater muscle contraction (Frank-Starling’s law)
how increased preload affects PV loop
1st portion ends at greater vol and higher P. Shifts the right part of the graph to the right. But all comes back to same ESV so greater stroke volume
how to increase preload (practically speaking)
squeeze capacitance veins, IV injection of fluid, receive blood
afterload two definitions
- pressure against which the heart contracts
- left ventricular wall stress during ejection
wall stress formula
ventr P x radius of ventr. div. (2 x wall thickness)
afterload is proportional to __________
left ventricular pressure
left ventricular load is considered to be _______
systolic arterial BP (diast BP + third of pulse pressure)
why consider that afterload is the MAP
bc normally, left ventricle systolic P = systolic arterial BP and aortic valve open
how increased afterload affects the PV loop
the 2nd portion (vertical isovol contraction) goes higher bc fighting against greater P so afterload is greater. P raises and falls back at ESPVR at greater volume so ESV increased
why greater aortic pressure leads to greater afterload
have to push harder to open the aortic valve
consequence of greater afterload on SV
SV reduced bc EDV unchanged and ESV increased
why ESV increases when afterload increased
greater afterload results in less shortening of the ventricle
2 clinical conditions where find high afterload
hypertension, aortic valve stenosis
contractility def
inherent strength of heart’s contraction
SS effect on tension-length cycle
shifts the curve upwards (for same muscle length, greater tension)
SS on PV loop
shifts ESPVR curve up and to the left (and is curved to the left a little). ESV is now lower (left part of the curve is now more to the left)
SS effect on SV and why
increased bc ESV decreased
ejection fraction formula + normal values
Stroke volume div. EDV x 100.
Normal EF: 55-70%
CO formula and determinants
CO=HR x SV
how body changes HR
SS and PSS affect the diastolic depolarization of the SA node
name of effects affecting HR and what we call it when SS vs PSS
chronotropic effects.
SS: positive chronotropic effect
PSS: negative chronotropic effect
name of effects affecting SV and 3 things that can do that
inotropic effects. (preload, afterload, contractility)
what we call the effect when preload, afterload and contractility increases
increased preload: positive inotropic effect
increased afterload: negative inotropic effect
increased contractility: positive inotropic effect
cardiac function curve plots what
CO as a function of cardiac filling pressure
how SS and PSS affect the cardiac function curve
shift it up or down
example of thing increasing cardiac filling (moving up on the cardiac function curve)
increased preload
cardiac output or cardiac function curve in the right atrium: plots what + shape
CO as function of right atrial P. sigmoidal shape. reach plateau at 3 mmHg and 12.5 L per min.
what shifts the right atrium cardiac function curve upwards
increased HR, contractility and decreased afterload (decreased BP and TPR)
right atrium cardiac fct curve shifted down is said to be ______ and shifter up is called _______
hypoeffective vs hypereffective
give 3 main imaging techniques to assess cardiac function and CO
Echography (ultrasound), cardiac angiography, radionuclide ventriculography (or MUGA: multigated acquisition scan)
how cardiac angiography works
catheters placed in right or left ventricle, inject radio-opaque medium
how radionuclide ventriculography works
IV injection of radioactive isotope, binds to RBCs, measure intensity of radiation at ventricles during cardiac cycle
other heart imaging technique to assess cardiac function and CO
PET scans, CT angiograms, cardiac MRI
Fick’s principle (gross formula)
amount of substance consumed by an organ is equal to blood flow rate x (what goes in organ - what goes out organ)
application of Fick’s principle to get CO
CO = oxygen consumed by the lung div (arteriol O2 - mixed venous O2). (200 div by (200-160))
To apply Fick’s principle, how to get O2 consumed
special machine for that
To apply Fick’s principle, how to get arterial O2
puncture in any artery
To apply Fick’s principle, how to get mixed venous O2
catheter to go to pulmonary artery or right ventricle
normal values in the calculation of CO using Fick’s principle
200 div. (200 - 160) = 5L per min
thermodilution method used for what
measuring CO
thermodilution method principle
saline of known temperature injected through catheter in right atrium. tip of catheter in pulm artery registers Temp change. CO can be calculated
how thermodilution results presented and interpreted
graph of amount of cold as function of time. greater surface area: lower CO. smaller SA: greater CO
