The heart pump Nov1 M2 Flashcards by Django E.

what S1 (1st heart sound) corresponds to

closure of the AV valves (tricuspid and mitral) during systole

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what S2 corresponds to

closure of seminular valves (aortic and pulmonic) at start of diastole and start of isovolumetric relaxation

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seminular valves (2)

aortic and pulmonary valve

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S3 corresponds to what

heart sound when ventricular filling at diastole when blood hits the ventricle wal

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S3 heard where (2)

individuals with very good diastole or indiv. with heart failure

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why hear S3

because vacuum created by ventricle relaxation

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ventricle relaxation passive or active

active (ATP dependent). put calcium back in SR

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S4 corresponds to what

atrial contraction when pumps blood in stiff ventricle (non compliant)

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S4 heard where

abnormal (pathologic) in patients with non compliant ventricle

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if had 4 heart sounds, in what order would hear them

S1, S2, S3, S4

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pressure volume loop. how to get that

plot left ventricular pressure as a function of ventricular volume

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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

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pressure volume loop 2nd part

isovolumetric contraction. pressure rises but volume stays the same (vertical rise)

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pressure volume loop 3rd part

aortic valve opens, ejection, ventricular volume falls to ESV. pressure rises but falls back a little

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pressure volume loop 4th part

from ESV, isovolumetric relaxation. vertical drop in P without change in volume. until mitral valves open

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why ventr pressure goes up when filling (increasing volume)

bc even though ventricles stretch, limited by pericardial cavity

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ESPVR def

end systolic pressure-volume relationship. (P and V relationship in ventricle at end of systole)

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ESPVR is an indicator of what

how strong the heart is

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ESPVR: what determines the moment when systole ends

is when aortic valve closes (when P aorta = P ventricle)

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EDPVR stands for what and what it does

end diastolic pressure-volume relationship. (P ventr as function of ventr. volume during filling of ventricle)

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EDPVR shape

follows first part of pressure volume loop and extends a bit higher and further to the right

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length-tension relationship or cardiac muscle length-tension cycle: what it is

ventricular muscle tension as a function of muscle length

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what curve does cardiac muscle length-tension cycle ressemble and why

the pressure volume loop bc ventricular volume and muscle length are related linearly

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how to see stroke volume on a PV loop

right vertical line minus left vertical line (EDV - ESV)

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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