Hemodynamics in Critical Care Module 2: Central Monitoring

Hemodynamics in Critical Care Module 2: Central Monitoring Hemodynamics in Critical Care Module 2: Central Monitoring

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Hemodynamics Beyond the Basics Hemodynamics in Critical Care Module 2: Central Monitoring This module will review – Right arterial pressures / central venous pressures – Pulmonary artery pressures – Systemic vascular resistance – Pulmonary vascular resistance UOHI Clinical Services 2009 Central Venous Pressure • Indication of Right Ventricular End Diastolic Volume – Preload of RV – Indication of fluid volume state CVP / RAP • The pressure in the right atrium, commonly referred to as the central venous pressure, measures how much pressure the blood returning to the heart is under. • The venous system has a high capacitance that means it can adapt to various volume states. • Veins, by virtue of thinner walls that lack muscles, stretch when the pressure increases. • This stretch allows the veins to hold more, but increases the venous pressure.

<strong>Hemodynamics</strong> Beyond the Basics<br />

<strong>Hemodynamics</strong> <strong>in</strong><br />

<strong>Critical</strong> <strong>Care</strong> <strong>Module</strong> 2:<br />

<strong>Central</strong> Monitor<strong>in</strong>g<br />

This module will review<br />

– Right arterial pressures / central venous pressures<br />

– Pulmonary artery pressures<br />

– Systemic vascular resistance<br />

– Pulmonary vascular resistance<br />

UOHI Cl<strong>in</strong>ical Services 2009<br />

<strong>Central</strong> Venous Pressure<br />

• Indication of Right Ventricular End Diastolic Volume<br />

– Preload of RV<br />

– Indication of fluid volume<br />

state<br />

CVP / RAP<br />

• The pressure <strong>in</strong> the right atrium, commonly<br />

referred to as the central venous pressure,<br />

measures how much pressure the blood return<strong>in</strong>g<br />

to the heart is under.<br />

• The venous system has a high capacitance that<br />

means it can adapt to various volume states.<br />

• Ve<strong>in</strong>s, by virtue of th<strong>in</strong>ner walls that lack muscles,<br />

stretch when the pressure <strong>in</strong>creases.<br />

• This stretch allows the ve<strong>in</strong>s to hold more, but<br />

<strong>in</strong>creases the venous pressure.


RAP<br />

• This can lead to swollen ankles and <strong>in</strong>creased<br />

jugular venous distention.<br />

• When more blood tries to enter the right atrium<br />

than the right atrium can hold, the result is an<br />

<strong>in</strong>crease <strong>in</strong> the CVP.<br />

• Thus CVP can be an <strong>in</strong>dicator of fluid status.<br />

• More blood volume causes the ve<strong>in</strong>s to stretch<br />

and <strong>in</strong>creases the <strong>in</strong>travenous pressure; less<br />

blood volume causes the ve<strong>in</strong>s to constrict and<br />

decreases the <strong>in</strong>travenous pressure.<br />

RAP<br />

• Though the CVP pressure can <strong>in</strong>form about fluid<br />

balance, it can be a later <strong>in</strong>dicator.<br />

• Excessive fluid takes awhile to <strong>in</strong>crease the CVP<br />

and frequently there are other <strong>in</strong>dicators such as<br />

rales or pulmonary edema first.<br />

• The CVP also represent the preload of the right<br />

ventricle. Preload is the amount of stretch <strong>in</strong> a<br />

chamber just before contraction.<br />

CVP/RAP<br />

• The more the stretch, the better the next<br />

contraction (up to a po<strong>in</strong>t of course).<br />

• Thus, if the CVP is elevated then the pressure <strong>in</strong><br />

the right ventricle, just before contraction is<br />

elevated.<br />

• Conversely, if the CVP is low, then the preload of<br />

the right ventricle is low and the next contraction<br />

will be less efficient<br />

CVP/RAP<br />

• Remember what is go<strong>in</strong>g on <strong>in</strong>side the heart just<br />

before the right ventricle contracts.<br />

• The tricuspid valve is open allow<strong>in</strong>g blood to<br />

move freely between the right atrium and right<br />

ventricle.<br />

• Therefore, the pressure <strong>in</strong> the right atrium and<br />

right ventricle should be identical, s<strong>in</strong>ce they are<br />

openly connected.


CVP/RAP<br />

• The CVP is reported as a mean pressure<br />

measurement, not a systolic and diastolic as other<br />

pressures we discuss.<br />

• Normal range for the CVP varies from textbook to<br />

textbook, but a good range is 2 to 6 mmHg.<br />

CVP/RAP<br />

There are many potential causes of CVP elevation;<br />

• fluid overload,<br />

• right heart failure,<br />

• (late) left heart failure<br />

• tricuspid stenosis. which reduces the output of the<br />

right ventricle leav<strong>in</strong>g it too full to receive all the<br />

blood from the right atrium result<strong>in</strong>g <strong>in</strong> <strong>in</strong>creased<br />

CVP.<br />

CVP/RAP<br />

• Pulmonary embolism, which also reduces the<br />

output of the right ventricle as above caus<strong>in</strong>g<br />

<strong>in</strong>creased CVP.<br />

• Pericardial tamponade –<br />

– the entire heart is under <strong>in</strong>creased pressure<br />

due to the constriction of the pericardium.<br />

– This allows less blood to be pumped forward,<br />

not because of the cardiac dysfunction, but<br />

simply because of the constriction.<br />

CVP/RAP<br />

• Differentiat<strong>in</strong>g between each of these causes<br />

relies on <strong>in</strong>terpret<strong>in</strong>g all the hemodynamic<br />

<strong>in</strong>formation at our disposal and a careful<br />

assessment of the patient.


CVP/RAP<br />

Waveform - CVP<br />

• Actually 3 separate waves<br />

– a wave – atrial systole<br />

– c wave – peak at open<strong>in</strong>g of tricuspid valve<br />

– v wave – ventricular systole<br />

a wave<br />

x descent<br />

c wave<br />

v wave<br />

y descent<br />

Rise <strong>in</strong> pressure due to atrial contraction.<br />

a waves are larger <strong>in</strong> the presence of any resistance to<br />

RV fill<strong>in</strong>g, (tricuspid stenosis, RV failure, cardiac<br />

tamponade) because resistance will <strong>in</strong>crease pressure<br />

as the atrium attempts to contract and eject blood.<br />

Fall <strong>in</strong> pressure due to atrial relaxation.<br />

Rise <strong>in</strong> pressure due to ventricular contraction and<br />

bulg<strong>in</strong>g of the closed tricuspid valve.<br />

Rise <strong>in</strong> pressure dur<strong>in</strong>g atrial fill<strong>in</strong>g.<br />

Fall <strong>in</strong> pressure due to the open<strong>in</strong>g of the tricuspid<br />

valve and the beg<strong>in</strong>n<strong>in</strong>g of ventricular fill<strong>in</strong>g.<br />

CVP/RAP Waveform<br />

CVP/RAP Waveform


Measur<strong>in</strong>g CVP<br />

Measur<strong>in</strong>g CVP<br />

Measur<strong>in</strong>g CVP<br />

Mov<strong>in</strong>g from CVP to PA Measurements…<br />

• CVP can be measured via a central l<strong>in</strong>e such as a<br />

<strong>in</strong>troducer or the distal port of a triple lumen<br />

catheter<br />

• It can also be obta<strong>in</strong>ed via a PA catheter<br />

• Pressures measurements further forward from the<br />

CVP are usually obta<strong>in</strong>ed via a PA catheter<br />

(sometimes called a Swan-Ganz catheter)


Pulmonary Artery Pressures<br />

Why <strong>in</strong>sert a PA catheter<br />

• Means to evaluate fluid status<br />

– Indicator of preload<br />

• Means to evaluate LV function<br />

– PAOP, PCWP, wedge<br />

• Means to evaluate CO measurement<br />

– Thermodilution technique<br />

– Intermittent or cont<strong>in</strong>uous<br />

PA Catheter<br />

• Multi-lumen, polyv<strong>in</strong>ylchloride catheters with balloon<br />

at the tip<br />

• Flow directed catheter<br />

• Inflation of balloon ensures that blood flow will move<br />

the catheter forward <strong>in</strong> the direction of blood flow<br />

• Typically bonded with hepar<strong>in</strong><br />

• Lumens from 2-7<br />

• Length from 60-110 cm<br />

• Size from 4-8 French<br />

PA Catheter<br />

PA Catheter Insertion<br />

• Most PA catheters have 4 lumens<br />

• Prior to <strong>in</strong>sertion<br />

– Balloon lumen for <strong>in</strong>flation<br />

– Flush all lumens with solution<br />

– Distal lumen <strong>in</strong> PA<br />

– Check <strong>in</strong>tegrity of balloon<br />

– Proximal lumen <strong>in</strong> RA – drug <strong>in</strong>fusion, CVP<br />

– Always deflate passively!<br />

monitor<strong>in</strong>g<br />

– Prepare fluid filled system that has been<br />

– Thermistor to measure blood temperature<br />

leveled and zeroed<br />

• Other lumens may be used for<br />

– Connect to appropriate lumens<br />

– Temporary transvenous pac<strong>in</strong>g<br />

• PA distal – PA pressures<br />

– Measurement of RVEDV and RVEF<br />

• Proximal <strong>in</strong>fusion – CVP<br />

– Cont<strong>in</strong>uous measurement of CO and SvO 2 • Proximal <strong>in</strong>jectate – CO device


PA Catheter<br />

PA Catheter Insertion<br />

PA Catheter Insertion<br />

PA Catheter Insertion<br />

• Waveform at distal tip visualized cont<strong>in</strong>uously<br />

(make sure the stopcocks are turned the right way!)<br />

• Balloon fully <strong>in</strong>flated when CVP wave is visualized<br />

• Catheter advanced with balloon <strong>in</strong>flated – blood<br />

flow will carry or “float” the catheter through RA, RV<br />

and <strong>in</strong>to PA<br />

• Be sure to use your<br />

handout to become<br />

familiar with how the<br />

trac<strong>in</strong>g appear as the<br />

catheter moves thru the<br />

heart


Pulmonary<br />

Wedge Pressure<br />

Pulmonary<br />

Wedge Pressure<br />

Trac<strong>in</strong>g from RA<br />

Trac<strong>in</strong>g as catheter moves from RA TO RV<br />

Pulmonary<br />

Wedge Pressure<br />

Pulmonary<br />

Wedge Pressure<br />

Trac<strong>in</strong>g as balloon is <strong>in</strong>flated for PWP


Pulmonary Right Pulmonary Ventricle Atrium Artery<br />

Wedge Pressure<br />

Waveforms - PA<br />

• Changes <strong>in</strong> waveform as PA catheter is advanced<br />

from the right atrium, rt ventricle <strong>in</strong>to pulmonary<br />

artery<br />

If there is no lung or<br />

mitral valve disease, the<br />

PAD and PWP are<br />

look<strong>in</strong>g forward <strong>in</strong>to the<br />

left ventricle and can tell<br />

us the LVEDP<br />

Trac<strong>in</strong>g as balloon is <strong>in</strong>flated for PWP<br />

Waveforms - PA<br />

Waveforms - PA<br />

• The PAP is constantly monitored by the distal port<br />

of the PA catheter.<br />

• The pulmonary artery systolic pressure (PAS)<br />

approximates the systolic pressure <strong>in</strong> the RV, but<br />

the pulmonary diastolic pressure (PAD) is higher,<br />

and the waveform less steep.<br />

• The PA waveform <strong>in</strong>cludes a diastolic notch which<br />

represents closure of the pulmonic valve.<br />

• In the absence of lung or mitral valve disease, the<br />

PAD approximates the pulmonary artery wedge<br />

pressure (PAWP) and can, therefore, aid <strong>in</strong><br />

evaluation of preload without wedg<strong>in</strong>g the<br />

catheter.


PA Pressures<br />

• The pulmonary artery pressure is reported as a<br />

systolic and a diastolic number.<br />

• The normal range for the systolic PAP is 12 - 25<br />

mmHg.<br />

• There is variation <strong>in</strong> the normal range <strong>in</strong> various<br />

textbooks<br />

• The diastolic PAP normal range is 7 to 15 mmHg..<br />

• The mean PAP pressure has a normal range of<br />

10 to 15 mmHg.<br />

• A typical read<strong>in</strong>g for the PA pressure is 20/12 with<br />

a mean of 13.<br />

PA Pressures<br />

• The pulmonary artery pressures measure the<br />

resistance of blood flow through the lungs.<br />

• Aga<strong>in</strong> fluid overload, left heart failure, constrictive<br />

pericarditis, and pulmonary embolism can all<br />

cause the PAP to <strong>in</strong>crease, but tricuspid and<br />

pulmonic valve stenosis will decrease the PAP<br />

because less blood can be ejected from the right<br />

ventricle.<br />

• The same effect occurs with right ventricular<br />

failure, the lack of blood be<strong>in</strong>g pushed <strong>in</strong>to the<br />

pulmonary artery will decrease the PAP read<strong>in</strong>gs.<br />

PA Pressures<br />

• Anyth<strong>in</strong>g that <strong>in</strong>creases the PA pressures will also<br />

lead to elevated CVP pressures, because the<br />

pressure will be transmitted back to the right<br />

ventricle when the pulmonic valve is open.<br />

• And, once the right ventricular pressures are<br />

<strong>in</strong>creased the pressure will be transmitted back to<br />

the right atrium when the tricuspid valve is open.<br />

• But, anyth<strong>in</strong>g that <strong>in</strong>creases the right atrial or right<br />

ventricular pressures will not necessarily <strong>in</strong>crease<br />

the PA pressures.<br />

• This is helpful <strong>in</strong> diagnos<strong>in</strong>g the cause of the<br />

pressure problems<br />

PWP or PAD<br />

• The PAOP, colloquially referred to as "the wedge",<br />

gives valuable <strong>in</strong>formation about fluid status with<br />

respect to the left side of the heart.<br />

• When this is documented, compare it to the<br />

pulmonary artery diastolic (PAD) pressure.<br />

• They should differ by only a few po<strong>in</strong>ts, with the<br />

PAD be<strong>in</strong>g about 2 to 4 mmHg higher than the<br />

PAD.<br />

• If the PAD is less than 25 mmHg and <strong>in</strong> the<br />

absence of lung or valvular problems, it is a<br />

adequate reflection of the POAP and can be<br />

used <strong>in</strong> calculations and <strong>in</strong>dication of LVEDP.


PWP or PAD<br />

• When the PAC balloon is <strong>in</strong>flated, the pressures<br />

from the right side of the heart can no longer<br />

reach the tip of the catheter.<br />

• The tip of the catheter now measures the<br />

pressures <strong>in</strong> front of the catheter <strong>in</strong> the pulmonary<br />

artery.<br />

• But, the pressure <strong>in</strong> the pulmonary artery <strong>in</strong> front<br />

of the catheter is really the pressure from the<br />

pulmonary ve<strong>in</strong>s push<strong>in</strong>g back on the blood <strong>in</strong> the<br />

pulmonary artery.<br />

PWP or PAD<br />

• The pressure push<strong>in</strong>g back <strong>in</strong>to the pulmonary<br />

ve<strong>in</strong>s, comes from the left atrium.<br />

• Therefore, a catheter <strong>in</strong> the right side of the heart,<br />

can measure pressures <strong>in</strong> the left side of the<br />

heart.<br />

• There are some caveats however….. If the patient<br />

has pulmonary hypertension or pulmonary<br />

embolism, conditions that specifically alter blood<br />

flow from the right side of the heart to the left side,<br />

then the PAOP does not accurately reflect left<br />

sided pressures<br />

PWP or PAD<br />

• That said, if the PAOP accurately reflects the left<br />

atrial pressure, then we can actually measure the<br />

pressure <strong>in</strong> the left ventricle - if the mitral valve is<br />

open.<br />

• Remember, if two areas of the heart are openly<br />

connected, the pressure will quickly equalize <strong>in</strong><br />

the two chambers.<br />

• If the pressure <strong>in</strong> the left atrium was higher then<br />

the pressure <strong>in</strong> the left ventricle when the mitral<br />

valve is open, then blood would move from the<br />

higher pressure area <strong>in</strong>to the lower pressure area<br />

and vice versa.<br />

PWP or PAD<br />

• Therefore, we can measure the pressure <strong>in</strong> the<br />

left ventricle as long as the mitral valve is open.<br />

And, when is the mitral valve open? - dur<strong>in</strong>g<br />

diastole, as the left ventricle is fill<strong>in</strong>g with blood.<br />

• Therefore, the pressure the PAD/PAOP is<br />

measur<strong>in</strong>g is actually the left ventricular pressure<br />

dur<strong>in</strong>g diastole, or Left Ventricular End Diastolic<br />

Pressure (LVEDP)!!!<br />

• This pressure actually gives us preload for the left<br />

ventricle, which is directly related to the amount of<br />

stretch the left ventricle has just before it contracts


PWP or PAD<br />

• This is the first <strong>in</strong>dicator of fluid imbalances.<br />

• If the PAD / PAOP is too high, then the pressure<br />

<strong>in</strong> the left ventricle dur<strong>in</strong>g diastole is too high.<br />

• This means that the heart is hav<strong>in</strong>g difficulty<br />

pump<strong>in</strong>g the blood it receives forward.<br />

• In general, this occurs due to fluid overload, or<br />

heart failure of the left ventricle.<br />

• This change occurs as soon as the fluid level<br />

starts to rise and, therefore, is a better <strong>in</strong>dicator<br />

than the CVP.<br />

PWP or PAD<br />

• If the PAD / PAOP is too low, this usually means that<br />

dehydration or volume loss is present.<br />

• The fluid loss can be relative or actual.<br />

• In sepsis fluid leaks from the blood vessels and<br />

enters the <strong>in</strong>terstitial spaces.<br />

• This will cause the PAD / PAOP to decrease as less<br />

blood returns to the heart, specifically the left<br />

ventricle, caus<strong>in</strong>g left ventricular preload to<br />

decrease.<br />

• If the fluid loss is actual, as <strong>in</strong> dehydration or<br />

significant bleed<strong>in</strong>g, then the result to the PAOP is<br />

the same - a decrease.<br />

Cardiac Output<br />

• Cardiac output can be measured with the<br />

pulmonary artery catheter us<strong>in</strong>g a method known<br />

as thermodilution.<br />

• Thermodilution refers to <strong>in</strong>ject<strong>in</strong>g fluid, of a known<br />

temperature, and measur<strong>in</strong>g the effect on the<br />

blood as it travels past the pulmonary artery<br />

catheter tip.<br />

• All PACs have a thermistor, which is basically a<br />

temperature measur<strong>in</strong>g device<br />

Cardiac Outputs<br />

• If you <strong>in</strong>ject room temperature D5W <strong>in</strong>to the<br />

<strong>in</strong>jectate port of the pulmonary artery catheter,<br />

then the temperature of the blood will decrease by<br />

an amount related to the relative volumes of the<br />

<strong>in</strong>jected fluid to the amount of blood <strong>in</strong> the heart.<br />

• The amount of time for the temperature of the<br />

blood to return to normal is directly related tot he<br />

cardiac output.<br />

• When the cool D5W is <strong>in</strong>jected <strong>in</strong> the heart, the<br />

temperature of the blood is decreased.


Cardiac Outputs<br />

• Then the heart contracts and ejects a certa<strong>in</strong><br />

percentage of the cooler blood, say 50%.<br />

• Now an equal amount of new, body temperature<br />

blood, mixes with the cooled blood that is left.<br />

• Then the heart contracts aga<strong>in</strong> and ejects 50% of<br />

this slightly warmer blood.<br />

• This cycle happens over and over aga<strong>in</strong>,<br />

contraction ejects cooled blood and then adds<br />

warmer blood to the mix.<br />

Cardiac Outputs<br />

• How long the process takes to <strong>in</strong>crease the blood<br />

temperature back to pre-<strong>in</strong>jection levels tells us<br />

how fast the heart is pump<strong>in</strong>g blood out of the<br />

heart - the cardiac output<br />

• This temperature change can be represented as a<br />

graph of the temperature difference between the<br />

pre-<strong>in</strong>jection blood and the post-<strong>in</strong>jection blood<br />

Cardiac Outputs<br />

• On this strip, you will see three examples of this<br />

graph.<br />

Cardiac Outputs<br />

• The curves first grow taller as the <strong>in</strong>jected blood<br />

gets ejected and passes the thermistor.<br />

• Then the curves beg<strong>in</strong> to grow smaller slowly as<br />

progressively warmer blood beg<strong>in</strong>s to pass by the<br />

temperature sensor.<br />

• The height of the curve represents the change <strong>in</strong><br />

temperature and the length of the curve<br />

represents how much time has passed.


SVR<br />

• Systemic vascular resistance, SVR for short,<br />

measures the resistance to eject<strong>in</strong>g blood from<br />

the left ventricle. It is a calculated value that is<br />

given by the formula<br />

• We can calculate cardiac output and can measure<br />

CVP and MAP (mean arterial pressure).<br />

SVR<br />

• This value is effected by total blood volume and<br />

artery size.<br />

• Dilated arteries decrease the resistance to<br />

eject<strong>in</strong>g blood and therefore lower SVR.<br />

• Conversely, constricted arteries cause the SVR to<br />

rise.<br />

• This is one way the body regulates cardiac output<br />

and blood pressure.<br />

SVR<br />

• Small changes <strong>in</strong> the diameter of a blood vessel<br />

has dramatic effects on the pressure needed to<br />

push blood through that artery.<br />

• If you double the size of the artery, you need<br />

1/16th of the pressure to push blood through it.<br />

• If you cut the artery size <strong>in</strong> half, then you need 16<br />

times as much pressure to get the blood through<br />

that artery.<br />

PVR<br />

• Pulmonary Vascular Resistance<br />

– Tells us how hard the right heart has to work to<br />

get blood through the lungs and back to the left<br />

heart<br />

Mean pulmonary arterial Pressure -PWP<br />

Pulmonary Vascular Resistance = x 80<br />

Cardiac Output<br />

• Normal values range from 20-120 dynes/sec/cm -5<br />

• Issues that may <strong>in</strong>crease pulmonary vascular<br />

resistance and <strong>in</strong> turn right ventricular afterload<br />

<strong>in</strong>clude pulmonary emboli, pulmonary edema,<br />

sepsis, acidosis, hypoxemia, pulmonary<br />

hypertension and some congenital or valvular heart<br />

diseases.


PVR<br />

• Factors that may decrease PVR <strong>in</strong>clude the use<br />

of pulmonary vasodilator drugs or gases and the<br />

correction of hypoxemia or acidemia.<br />

You’re done !!<br />

• Take a moment to go to Classmarker and<br />

challenge yourself with a quiz

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