Hemodynamics advanced orientation, july 2008 - copy

Advanced HemodynamicsAdvanced Hemodynamics

Kathleen Brownrigg, RN, MNKathleen Brownrigg, RN, MNPediatric Critical Care UnitPediatric Critical Care Unit

ObjectivesObjectives

Discuss invasive monitoring linesDiscuss invasive monitoring lines

Review IndicationsReview Indications

Understand normal hemodynamicsUnderstand normal hemodynamics

Gain competency in monitoringGain competency in monitoring

Interpret hemodynamic dataInterpret hemodynamic data

Objectives Understand hemodynamic variations of congenital cardiac Understand hemodynamic variations of congenital cardiac

diseasedisease

Review hemodynamic waveforms and intracardiac pressuresReview hemodynamic waveforms and intracardiac pressures

Describe complications of invasive linesDescribe complications of invasive lines

Correlate hemodynamic data with clinical assessmentCorrelate hemodynamic data with clinical assessment

Discuss the impact of preload, afterload, contractility and Discuss the impact of preload, afterload, contractility and ventricular complianceventricular compliance

History

1st measurements in 1773 by Stephen Hale, an English theologian/scientist and assistant

Measuring directly 1st mean BP on an unanesthetized horse

Measurement of BP evolved slowly

Cardiac OutputCardiac Output

Measure of performanceMeasure of performance

Volume of blood ejected in 1 minVolume of blood ejected in 1 min

C.O. = HR X SVC.O. = HR X SV

Varies with sizeVaries with size CI = CI = COCO BSABSA

Heart RateHeart Rate

Vital for good cardiac performanceVital for good cardiac performance

Children are less able to vary stroke volume as their Children are less able to vary stroke volume as their myocardial performance is working near max under myocardial performance is working near max under basal conditionsbasal conditions

SV is less dynamic – HR influences CO to a greater SV is less dynamic – HR influences CO to a greater extent that in adultsextent that in adults

Tachycardia – shortening of diastolic component of Tachycardia – shortening of diastolic component of cardiac cycle = 30% of total cycle timecardiac cycle = 30% of total cycle time

Indications For HemodynamicMonitoring

Shock states: Cardiogenic, hypovolemic, distributive

Surgical patients

Respiratory patients

Multiple trauma

Invasive Monitoring

Provides objective quantitative data:Provides objective quantitative data:

Cardiac output Cardiac output PreloadPreload AfterloadAfterload Rt & Lt heart functionRt & Lt heart function Assessment of intracardiac shuntingAssessment of intracardiac shunting Assessment of pharmacologic responseAssessment of pharmacologic response

Risk vs Benefit

Necessity vs risk assessment Necessity vs risk assessment

EmbolismEmbolism

Vessel thrombosis Vessel thrombosis

Vessel patency - palliative cavopulmonary Vessel patency - palliative cavopulmonary connection, cardiac transplantation and repeated connection, cardiac transplantation and repeated biopsybiopsy

Goal

Increase stroke volume

Increase cardiac output

Maximize filling pressures

Decrease pulmonary congestion

Monitoring

Tailored to the individual infant, defect & reparative surgical intervention- Line placement – ie left radial art line and repair of - Line placement – ie left radial art line and repair of

coarctation with subclavian flap is inappropriatecoarctation with subclavian flap is inappropriate

Information outweighs risks/complications – remove lines ASAP

Line should be transduced for a waveform prior to potent or corrosive drugs. i.e. cyanosed & hypotensive patient, …..color or force of ejection may not be helpful in determining ART vs venous line

Invasive Monitoring

Oxygenated blood (ABP, UAC, Pulmonary veins - LAP)Oxygenated blood (ABP, UAC, Pulmonary veins - LAP)

Deoxygenated blood (CVL, PA Lines, UVC)Deoxygenated blood (CVL, PA Lines, UVC)

Requires a fluid filled system (catheter & tubing)

Requires a pressure transducer to transmit one energy form to another – ie physical energy to an electrical signal that is amplified

Transducing Solutions

ART Lines: 0.9 NaCl with 100 units of Heparin/50 ml

Run at 1.5 to 2ml/hr. Cardiac neonate rate 1.0 ml/hr

All other: D5W & 0.2 NaCl with 100 units of Heparin/ 50 ml

Run at 2ml/hr (minimum rate 1.5 ml/hr). May decrease to 0.5 ml/hr if sufficient fluid infusing through line to keep vein open.

DO NOT TURN TRANSDUCING FLUID OFFDO NOT TURN TRANSDUCING FLUID OFF completely - completely - stagnation of fluid in transducerstagnation of fluid in transducer

Proper Leveling/Rezeroing Point?

Must be leveled to an anatomically consistent point

Phlebostatic axis provides an external reference point

Reference point that approximates the anatomic level of the atria and PA

Ensures accuracy of readings

Must be zeroed to eliminate effects of hydrostatic & atmospheric pressures

Zeroing stopcock should be used

Phlebostatic Axis

Midpoint between the anterior and posterior surfaces of the chest at the 4th intercostal space midaxillary line

Zeroing/Calibrating

Inaccurate transducer position can result in large errors in reading!!!!!

Zeroing

Zeroing

Causes of Error?

Air bubbles in the system = underestimation of systolic pressure and overestimation of diastolic pressure

Blood clots

Use of non-compliant tubing

Tighten loose fitting connections

Catheter lodged again vessel wall

Improper zero

Interpretive

Arterial Pressures?

Moment by moment pressure

Visual display of systolic, diastolic and MAP

MAP = 2X(DAP) + SAP

3

Dicrotic Notch

Intrathoracic LinesIntrathoracic Lines

Directly positioned at time of surgeryDirectly positioned at time of surgery

RA, LA PA, RVRA, LA PA, RV

Fixed to the thorax by a sutureFixed to the thorax by a suture

Maintained with 1.5-2.0 ml/hrMaintained with 1.5-2.0 ml/hr

RA LinesRA Lines Information about:Information about:

systemic venous returnsystemic venous return

vascular volumevascular volume

right heart eventsright heart events

Reported as a mean pressureReported as a mean pressure

Ideal location is within the body of RA where Ideal location is within the body of RA where venous blood return is mixedvenous blood return is mixed

RA line is a low pressure lineRA line is a low pressure line

RA Lines

Reflects preload or right ventricular end diastolic Reflects preload or right ventricular end diastolic pressure (RVEDP)pressure (RVEDP)

Placed through RA appendage during surgeryPlaced through RA appendage during surgery

oror

Threaded into the RA by venous cannulation or Threaded into the RA by venous cannulation or umbilical venous lineumbilical venous line

RA Line

Low RAP: hypovolemiaLow RAP: hypovolemia

waveform dampeningwaveform dampening

faulty positioning of transducerfaulty positioning of transducer

line placement in the coronary line placement in the coronary

sinus or low in IVCsinus or low in IVC

RA Line

High RAP: RV dysfunction

Tricuspid stenosis or insufficiency

Hypervolemia

Tamponade

Constrictive pericarditis

Pericardial effusion

LV to RA shunt

Pulmonary hypertension

LA Catheters

Provides a measurement of pulmonary venous pressure

Indicates systemic volume, LV preload, LV function

Placement: Posteriorly through the wall of LA at the junction of superior pulmonary vein and advanced across the LA

Xray display a straight line across the chamber

LA Catheters Low pressure: hypovolemia

Increased LAP:

Deep inspiration

PEEP

Hypervolemia

Mitral valve insufficiency

Loss of AV conduction

Ventricular dysfunction

Coronary artery occlusion

Pericardial effusion/tamponade

Cardiac Output Cardiac Output is a product of stroke volume X HR SV 60-130 ml Adult Factors affecting SV: preload, afterload contractility

Cardiac Index: adjusts CO to individual persons body size = blood flow relative to a square meter of body surface area.

1/3 cardiac cycle – consuming O2 2/3 diastolic & perfusing coronary arteries Cardiac index is highest in childhood and diminishes with age

Principles of Hemodynamics

Blood Pressure = C.O. X SVRBlood Pressure = C.O. X SVR

C.O. & SVRC.O. & SVR have an inverse relationship: If blood pressure drops, SVR increases to compensate = equilibrium

SVR is the strongest component regulating BP

A vasoconstrictor has a greater effect than an inotrope

Cardiac medications manipulate the:

Contractility (improve/depress)Contractility (improve/depress)

Preload (increase/decrease)Preload (increase/decrease)

Afterload (increase/decrease)Afterload (increase/decrease)

Alpha Adrenergic Receptors

Receptors in the peripheral and coronary arteries.

Peripheral vasoconstriction - skin, lungs, GI tract, and kidneys

Increases sweating

Dilates pupils

Norepinephrine, Epinephrine, DopamineNorepinephrine, Epinephrine, Dopamine

Beta 1 Adrenergic Beta 1 Adrenergic ReceptorsReceptors

B1:B1: Receptors in the heart, lungs and coronary arteries. (lesser in vessels)

Found largely in the heart

Increases: HR, contractility, conductivity

Norepinephrine, Epinephrine, Dopamine, Dobutamine, Norepinephrine, Epinephrine, Dopamine, Dobutamine, Isuprel Isuprel

Beta 2 Adrenergic ReceptorsBeta 2 Adrenergic Receptors

Found largely in the lungs

Bronchodilation

Peripheral vasodilation: skeletal muscles, heart and lungs

Arteriolar dilation = O2 delivery to the cells

Adrenalin, Isuprel, VentolinAdrenalin, Isuprel, Ventolin

Caution: B-Blockers: Propanolol, Esmolol, Labetolol, Caution: B-Blockers: Propanolol, Esmolol, Labetolol, AtenololAtenolol

Preload

Preload:Preload: End diastolic stretch of the muscle fibres. Vol and pressures in ventricle just prior to systole

Frank Starling principleFrank Starling principle: The greater the muscle fibres are stretched in diastole, the more they will shorten and with > force in systole

If preload increases so does C.O. to an optimum level

Preload

The ideal preload is associated with optimal cardiac output

What is that norm for your patient??????

Influencing factors: circulating blood volume, distribution of blood volume, atrial contraction

Estimating preload: PAD

LAP

RAP

AfterloadAfterload

ResistanceResistance to blood flow as it leaves the ventricles

Major influences – vascular compliance & outflow obstruction

A function of: Arterial pressure

Ventricular size

An increase in vascular resistance (PVR or SVR)(PVR or SVR) results in an increased contractility in order to maintain: stroke volume and C.O

Increase in SVR or PVR - more energy required for ejection - myocardial O2 demand increases myocardial O2 demand increases

AfterloadAfterload

Systemic hypertension (functional)

Pulmonary hypertension (functional)

Aortic stenosis/Coarctation (structural)

Pulmonary stenosis (structural)

SVRSVR

SVR (Woods units) = MAP – Mean RAP(CVP)

Cardiac output

= 10 – 15 Woods units

SVRI (dynes-sec-cm -5) = MAP – Mean RAP(CVP) X 80

Cardiac index

= 800-1600 dynes/sec/cm-5

PVR

PVR (Woods units) = MAP – Mean RAP

Cardiac output

= 1-3 Woods units over 8 wks of age

8-10 Woods units < 8 weeks of age

PVRI (dynes-sec-cm -5) = MAP – Mean PCWP (or LA ) X 80

Cardiac index

= 80-240 80-240 dynes/sec/cm-5

Factors Causing Increased Factors Causing Increased PVRPVR

Alveolar hypoxia and PA vasoconstriction: Alveolar hypoxia and PA vasoconstriction: hypoventilationhypoventilationETT obstruction ETT obstruction pneumothoraxpneumothorax

Obstruction to flow: Obstruction to flow: pulmonary venous obstructionpulmonary venous obstructionmitral valve stenosis, mitral valve stenosis, severe left ventricular failure severe left ventricular failure

Potential Vasoconstrictors for Potential Vasoconstrictors for PVRPVR

Potential VasoconstrictorsPotential VasoconstrictorsAcidosisAcidosisBody temperature – hypothermiaBody temperature – hypothermiaStimulation – PainStimulation – Pain

Potential Vasodilators:Potential Vasodilators:Good oxygenationGood oxygenationAlkalosisAlkalosisMild hyperventilationMild hyperventilationSedationSedationInhaled nitric oxideInhaled nitric oxide

Contractility Inotropic state of the muscle. The ability of the myofibrils Inotropic state of the muscle. The ability of the myofibrils to shorten in length and produce a contraction for any given to shorten in length and produce a contraction for any given preload and afterload.preload and afterload.

Preload & afterload

Drugs – concentrations of circulating catecholamines,

inotropic agents, pharmacologic depressants

Cardiac oxygenation

Physiological depressants: hypoxia, hypercapnia,

acidosis

Functional myocardium

Ionized Ca++

Contractility

Not measured directly

Use SWI (stroke work index) to assess ventricular contractility

SVI SVI 33-47 cm/m2/beat33-47 cm/m2/beat

RVSWI RVSWI 7-12 gm/m2/beat 7-12 gm/m2/beat (6 - 7 Curley)(6 - 7 Curley)

LVSWILVSWI 35-85 gm/m2/beat35-85 gm/m2/beat (50 - 62 Curley)(50 - 62 Curley)

If high:If high: B-blockers: Propanolol

If low:If low: +ve inotropes: Dopamine, Milrinone, Epinephrine

Normal Saturations

75%

70%

75%

95%

95%

75%

75%

35%Coronary sinus

May be falsely high or low depending on catheter placement or residual lesions

Step UpCorrelation of RA to PA sat with residual lesions

LA Saturations

Decreased LA O2 SAT:

- intrapulmonary shunting as a result of atelactasis, lung collapse, consolidation - R to L cardiac shunt

Can not really be assumed

Cardiac Function

Adequate C.O. and balance between:

O2 DELIVERY O2 DELIVERY & O2 Consumption or DEMANDO2 Consumption or DEMAND

If balance is altered then anaerobic glycolysis (lactic acidosis)

Blood leaves heart 100% O2 saturated

Tissue extraction is 25%

SvO2 (mixed venous oxygen saturation) is 75% (60-80%) ….blood returning to right side of heart

Tissue Metabolism

O2 Delivery

(DO2)

O2 Consumption

(VO2)

Systemic O2 balance is critical!Systemic O2 balance is critical!

Is it an O2 deliveryO2 delivery or tissue extractiontissue extraction problem?

An increase in O2 consumption(VO2) is usually seen 4 hrs post op due to a rise in central body temperature

SvO2 Monitoring: Too High

High O2 supplyHigh O2 supply: FiO2 too high

Low O2 demandLow O2 demand: Anesthesia/sedation - little muscle activity

Hypothermia lowers metabolic demands

Sepsis impairs utilization of O2 – early high output state

L to R shunt

PAPVD or TAPVD

LV-RA shunt

Aorto pulmonary collaterals

SvO2 > 80%SvO2 > 80%

SvO2 Monitoring: Too Low

Low O2 supplyLow O2 supply: Hypoxemia (lung disease or poor supply)Low cardiac outputCatheter position in the coronary sinus or low in IVC

High O2 demandHigh O2 demand: Consumption high (demand > supply)

Shivering, Seizures

Hyperthermia

Nursing activities

Pain, anxiety

SvO2 < 60%SvO2 < 60%

Conditions That Increase VO2

Minor Surgery 7%

Fever – for each degree rise 10%

Agitation 16%

Increased WOB 40%

Severe infection 60%

Multiple organ failure 20-80%

Shivering 50-100%

Burns 100%

Sepsis 50-100%

Darovic

Medications That Increase VO2

Norepinephrine (0.1-0.3 mcg/kg/min)

10-21%

Dopamine 5 mcg/kg/min 6%

Dopamine 10 mcg/kg/min 15%

Epinephrine 0.1 mcg/kg/min 23-29%

Ace inhibitors for systolic failure

Used when pump not strong enough or SVR too high

B blocker –slow hr and decrease O2 requirements.

Darovic

Procedures/Activities Increase VO2

Dressing change 10%

Nursing assessment 12%

ECG 16%

Physical exam 20%

Bath 23%

Chest Xray 25%

ET suctioning 27%

Turn 31%

Nasal intubation 25-40%

Darovic

Factors that Decrease VO2

Hypothermia (for each degree C)

10%

Morphine Sulphate 9-21%

Anesthesia 50%

Assist control ventilation 30%

Neuromuscular blockade Abolishes the increase in VO2 incurred by shivering

Darovic

Cardiac Function

If you have decreased C.O tissues, will extract more O2 so the MvO2 will drop

If there is a patch leak (ASD, VSD, AVSD) then MvO2 will increase

PA Catheters

Provides information about:

Mixed venous oxygen saturations

RV function

RVOT patency

Pulmonary vascular reactivity

Venous pressure in the lungs

Placement: via RVOT into main PA

Elevated PAP

Hypervolemia

Increased pulmonary blood flow with L to R shunt

Lung disease

Mitral stenosis

Obstructed TAPVD

Pulmonary embolus

Understanding Waveforms

Waveform analysis

Scale?

Modified StarlingCurve

Relationship between ventricular

filling pressure and stroke volume

Curve B

Normal Function

As PCWP increases – SV increases

Curve A –

Enhanced Sympathetic stimulation

Curve C & D – Depressed contractility – curve shifts to right. In response to an increased filling pressure only minimal augmentation of stroke volume and addition of appropriate pharmacology is required.

Volume administration and augmentation of preload improves stroke volume

Ventricular compliance refers to the distensibility of the ventricle and is related to the changes in volume

If the ventricle is compliant ie distensible then a large increase in LVEDV can be accommodated with min change in VEDP

Modified Starling Curve

LVEDP

The relationship between of ventricular filling volume and ventricular filling pressure to changes in stroke volume are not consistent between patients and are not the same over time in the same patient.

These relationships are prone to changes

Non-Compliant Stiff Ventricles

A noncompliant stiff ventricle such as a hypertrophic ventricle - even a small increase in ventricular end diastolic volume may produce significant increase in LVEDP

High filling pressures lead to pulmonary edema, increased systemic venous pressure on RV.

Intravascular Lines & Swan Ganz Catheters

EKG and Atrial WaveformEKG and Atrial Waveform

Record atrial pressure waveform & EKG Record atrial pressure waveform & EKG simultaneouslysimultaneously

a wave occurs at approx the same time as the QRSa wave occurs at approx the same time as the QRS

v wave occurs near the T wavev wave occurs near the T wave

A, C & V wavesA, C & V waves

The atria do not have systolic & diastolic pressuresThe atria do not have systolic & diastolic pressures

Mean atrial pressure is the average pressure in the Mean atrial pressure is the average pressure in the atrium during the cardiac cycleatrium during the cardiac cycle

3 positive deflections during each cardiac cycle – a, 3 positive deflections during each cardiac cycle – a, c & v c & v

A, C & V WavesA, C & V Waves

a – wavea – wave produced by atrial contractions during atrial produced by atrial contractions during atrial systolesystole

c – wavec – wave produced due to the rapid rise in ventricular produced due to the rapid rise in ventricular pressure in early systole, causing the AV valve leaflets to pressure in early systole, causing the AV valve leaflets to bulge back into the atria so that the atrial pressure bulge back into the atria so that the atrial pressure increases brieflyincreases briefly

v – wavev – wave produced by blood entering the atrium produced by blood entering the atrium during late systole. during late systole.

CVP & LAP

A wave

C wave

V wave

C wave is a notch on the a wave or may be absent

A & C & V waves

A waveA wave

V waveV wave

C waveC wave

Atrial Contraction Bulging of valve Atrial filling

into atria Ventricular contraction

* * *

A & C & V Waves

Atrial fibrillation = no A -wave

A & C & V Waves Usually atrial contraction (a-wave) produces a taller wave than ventricular filling (v-wave) in the RA and reverse in the LA

LAP A and V waves are a little away or delayed in comparison to RAP pressure waveforms.

Cannon A Waves

Right Side

Tricuspid AtresiaEbstein’sPulmonary StenosisPulmonary venous occlusive diseasePulmonary hypertensionVentricular hypertrophyVentricular dysfunction

Cannon waves occur when the atria contracts against a closed valve, loss of normal sinus rhythm

Cannon A Waves

Left Side

Mitral stenosisVSDPDAAortic stenosis

Cannon waves occur when the atria contracts against a closed valve, loss of normal sinus rhythm

Right side

Tricuspid regurgitation

ASD

Congestive heart failure

Cannon V Waves

Left side

Mitral regurgitation

CHF

Cannon V Waves

Mitral Valve Regurgitation

5 ½ yr old Ross Procedure

Mitral, trivial tricuspid and aortic regurgitation

LAP

VV V V VLAP

LAP

Mitral Regurgitation

Mitral Regurgitation & Cannon v- waves

LAPLAP

LAP

3 ½ yr Old Cardiomyopathy

RAP

ART

RAP

3 ½ yr old cardiomyopathy

Cannon A – poor ventricular function

Cannon V – tricuspid valve regurgitation

LA Waves

3 ½ cardiomyopathy awaiting a heart transplant

Cannon v due to mitral regurgitation

Cannon a waves due to ventricular failure

3

12

RV Line

2RV

RV

1

3

RVP 58/3 (Note subsytemic RV systolic pressures)

RV Line

RV

Infant

RV

ART

ART

33

11

11

2233

No dicrotic knotchNo dicrotic knotch

PAP WaveformPAP Waveform

PA waveform in the pulmonary artery – differs from PA waveform in the pulmonary artery – differs from the RVthe RV

PA diastolic pressure higher than RV – pulmonary PA diastolic pressure higher than RV – pulmonary valve closes preventing PA diastolic from becoming valve closes preventing PA diastolic from becoming lowerlower

Swan Ganz Catheter

4-5 lumens

1) RAP (right atrial pressure)

2) PAP (pulmonary artery pressure)

3) PCWP (pulmonary capillary wedge pressure)

4) Cardiac output measurement via thermodilution

5) Lumen for drug/fluid administration

Swan Ganz Catheters: Advantages

Allows for real time determination of systemic oxygen delivery and consumption

Invasive (right heart)

Measures pressures in the heart and in the lungs

Differentiates pulmonary disease vs left ventricular failure

Guides treatment: drugs/fluids

Multilumen balloon tipped catheter

PA Lines

PAP

X-ray of PA Line

The tip of the catheter should not be visible beyond the silhouette of mediastinal structures

Commonly in the right main PA

Swan Ganz: Complications

Pulmonary embolism

Thrombus formation

Infection

PA perforation

Dysrhythmias

Dislodged & wedged

Balloon bursts

Catheter kinked

Waveform Changes

5-10 mmHg 20-30 mmHg 20-30 mmHg 6-12 mmHg

5-10 6-12

Mean PAP (10-20) mmHg

PA Waveform

12 3

Swan Ganz

RAP

LAP slightly higher than RAP.

RAP can be used to assess volume and function in the healthy person as they correlate well….. but not one with cardiopulmonary dysfunction

Acidosis, hypoxemia, positive pressure ventilation at high pressures and CHD alter the relationship

RVP

Elevated in


Pulmonic stenosis

VSD

RV diastolic pressure elevated due to RV dysfunction

RV Catheters

RV line

PA catheter that slips back? Vs purposeful placement

Documentation of pressures and waveforms

Watch for ventricular arrhythmias

PAP

Elevated in pulmonary emboli

COPD

VSD

Increased PBF – L to R shunt

PA hypertension

Severe heart failure

PCWP

What Are Your Pressures?

PA Wedge (PWCP)PA Wedge (PWCP)

Left heart pressureLeft heart pressure Measured by the SWANMeasured by the SWAN Measures LVEDPMeasures LVEDP Read when inflated balloon lodges in a smaller branch Read when inflated balloon lodges in a smaller branch of the PA – occlusion of the branchof the PA – occlusion of the branch Pressure of the distal catheter will be the same as the Pressure of the distal catheter will be the same as the LALA In the absence of lung disease Wedge should be 1- 5 In the absence of lung disease Wedge should be 1- 5 mmHg < than PAD mmHg < than PAD

PAP to Wedge

End diastole

Dicrotic notch

Intentional or Not? Spontaneous wedging in the PA = pulmonary infarction!

11

33

22

PAD not equal PCWP Pulmonary diastolic pressure do not equal LVEDP

PCWP is a static reading during diastole and systole

When wedge higher consider ARDS in the face of high ventilator settings

> 4mm difference between PAD and wedge then likely not accurately measuring LVED but more likely the lung disease

Measure over again and compare to BP, and U/O

Identify which wedge get the best C.O/pt

Anatomy

PAD & PCWP Analysis

When PCWP is > true LVEDPWhen PCWP is > true LVEDP

Mitral stenosis

Myxoma

Mitral valve regurgitation

Pulmonary embolism0

Computation Constant

Thermodilution

Thermodilution

Errors

Quantity of injectate

Injection time

Rewarming of injectate

Calculating Equations

C.O.C.O. = HR X SV = 4-6 L/min

C.I.C.I. = C.O. = 3-5 L/min/m2

BSA

SVRSVR = MAP - RAP X 80 dynes/sec/cm -5

C.O.

PVR PVR = mPAP - PCWP X 80 dynes/sec/cm -5

C.O.

Cardiac Volumes

C.O.C.O. = 4-8 L/min

C.I.C.I. = 3-5 L/min Adult – 2.5-4 L/min

Stroke volumeStroke volume = 60 - 100 ml/beat

Stroke volume in childrenStroke volume in children 1.5 ml/kg/beat

Ejection fractionEjection fraction = > 60 %

Pressures

CVPCVP 5-10 mmHg LAPLAP 6-12 mmHg

RAPRAP 5-10 mmHg PCWPPCWP 6-12 mmHg

RVPRVP 15 - 25 mmHg MAPMAP (age related)

5-10

PAPPAP 15 - 30 mmHg

8-12

mPAPmPAP (10-20) mmHg or < 1/2 to 1/3 systemic

Making Sense of Pressures

Increased RAP:Increased RAP: Right ventricular failure

(>10 mm Hg)(>10 mm Hg) Hypervolemia

Tricupid stenosis/regurgitation

Pulmonary stenosis/regurgitation

Cardiac tamponade

Decreased RAPDecreased RAP Hypovolemia

(< 5 mm Hg)(< 5 mm Hg) Vasodilation


PCWP reflects LVEDP onlyonly when there is no obstruction (pulmonary disease or mitral valve disease)

Increased PCWP:Increased PCWP: Left ventricular failure

(>12 mm Hg)(>12 mm Hg) Hypervolemia

Mitral stenosis/regurgitation

Aortic stenosis/regurgitation

Cardiac tamponde

Decreased PCWPDecreased PCWP Hypovolemia

(< 6mmHg)(< 6mmHg) Vasodilation


ElevationElevation & Equalization of pressures: RAP = PCWP

Filling problemsFilling problems - tamponade/constriction

- restrictive cardiomyopathy

BEWARE!!BEWARE!!

Assessment of TamponadeAssessment of Tamponade

Increasing tachycardiaIncreasing tachycardia

AgitationAgitation

HypotensionHypotension

Elevated intracardiac pressuresElevated intracardiac pressures

Abrupt cessation of chest tube drainageAbrupt cessation of chest tube drainage

Cardiac arrestCardiac arrest

Systolic/Diastolic PAP

PA systolic pressure equals RV systolic pressure unless RVOT obstruction is present

PA diastolic pressure corresponds to LA pressure if no gradient exists across the mitral valve

Oxygen Saturation: Reflects total mixed venous sample

ShuntingShunting

Determination of L to R shunt by calculating Qp:Qs Determination of L to R shunt by calculating Qp:Qs (pulmonary to systemic blood flow ratio)(pulmonary to systemic blood flow ratio)

Uses saturation data from the intracardiac linesUses saturation data from the intracardiac lines

Qp:Qs = Qp:Qs = Art Sat – RA SatArt Sat – RA Sat

Pulm ven sat – PA satPulm ven sat – PA sat

Qp:Qs = Qp:Qs = 100 – 75100 – 75 = = 2525 Normal = 1:1Normal = 1:1

100 – 75100 – 75 25 25

Complications of Thoracic Complications of Thoracic LinesLines

InfectionInfection

HemorrhageHemorrhage

MalpositionMalposition

EntrapmentEntrapment

FragmentationFragmentation

EmbolusEmbolus

DeathDeath

Guidelines for Intrathoracic Line Removal

Volume available

Determine clotting factors

Stop Heparin infusion in preparation for removal

Assess patency of chest tubes

CVS removes

OBSERVE FOR CARDIAC TAMPONADE

PAP

PVR drops by 80 % after birthPVR drops by 80 % after birth

PVR progressively falls & reaches adult levels within a PVR progressively falls & reaches adult levels within a few weeksfew weeks

Pulmonary arteries are very reactive in neonatal period Pulmonary arteries are very reactive in neonatal period

Vasoconstriction due to alveolar hypoxia, acidosis, Vasoconstriction due to alveolar hypoxia, acidosis, over-distension of the alveoli, or hypothermiaover-distension of the alveoli, or hypothermia

Vasodilation is promoted by alveolar oxygenation, an Vasodilation is promoted by alveolar oxygenation, an alkalotic pHalkalotic pH

Wedged PA catheter• Occluded segment – looks through the non-active segment

PA Wedge

PA Wedge

If wedge waveform were to be on an incline = over wedging Balloon will be overdilated – build up of pressure within the flush system.

PA Line Wedged

312

PAP

PAP Wedged

PAP

PCWP

PCWP is used to assess: PCWP is used to assess:

Intravascular volume (preload)Intravascular volume (preload)

Function of the left ventricleFunction of the left ventricle

Is a measurement of the pressure in the left atrium

Is NOTNOT a measurement of left ventricular preload but is a reflection of LVEDP

Can reflect the pressure in the surrounding alveoli

Is NOTNOT a measure of capillary hydrostatic pressure

Is NOTNOT a transmural pressure

PAD & PCWP Analysis

When PAD is < LVEDPWhen PAD is < LVEDP

Left ventricular failure

Aortic valve regurgitation

PAD & PCWP analysis

When PAD = PCWPWhen PAD = PCWP

Increased PVR

Mitral valve disease


Pulmonary venous disease

High Peep >10mmHg

Cor pulmonale

Pulmonary embolism

Cardiac Output

Case 1

2 yr old post op cardiac surgical repair of VSD

HR HR 166/min

C.OC.O 3.0 SVRSVR 1712

CICI 1.8 PVRPVR 350

BPBP 60/35 PAPPAP 46/22

CVP CVP 16 RVSWIRVSWI 4

PCWPPCWP 22 LVSWILVSWI 21

Case 2

12 yr old patient who underwent a Ross Konno procedure for LVOT and aortic valve reconstruction

HR HR 136


CICI 2.2 PVRPVR 150




Case 3

16 yr old post op cardiac surgical repair of mitral valve

HRHR 166/min


CICI 2.1 PVRPVR 175

BPBP 70/48



Case 4

2 yr old previous AVSD repair at 4 weeks of age admitted with SOB post RSV.

HRHR 168


CICI 3.0 PVRPVR 385


CVP CVP 14 RVSWI RVSWI 5


Case 5A 10 yr old cardiomyopathic patient in critical care awaiting heart transplant. This is her hemodynamic data. She has a CVL, PA line, LA line. You have just returned from the cardiac catheterization lab and the following data is available for you to interpret.

HR HR 126

C.OC.O 10 SVRSVR 356

CICI 5.7 PVRPVR 302




Sepsis Patient

7 yr old sepsis patientGram negative septic shockMulti-organ failure: respiratory, renal, liverSvO2 = 75%Lactate of 2.2Vasopressin 0.0002 units/kg/hrEpinephrine .03 mcg/kg/min Dopamine 7.5 mcg/kg/min

Started on Milrinone .66 mcg/kg/min Nipride of 1.0 mcg/kg/min

Sepsis Patient

PAP = 37.8 deg. Temp

Esophageal = 37.2 deg. Temp

Wt 25 kg

Ht 126 cm

Sepsis 21:00 01:03 04.22 11:00

CO 3.87 6.29 6.27 2.07

CI 4.07 6.62 6.60 2.18

SI 30.97 48.3 47 15.7

SVRI 1060 918 787 2385

PVRI 314 85 194 550

HR 132 137 140 139

BP 110/59 148/76 123/63 116/74

PAP

(mean)

43/34 (37) 44/36 (31) 46/37 (32) 46/36 (31)

PCWP 21 29 21 21

RAP 19 17 16 21

SvO2 72 69 70 50

SVR 2511

PVR 579

SV 14.9

Intramural MI

14 yr old sudden loss of consciousness while playing sports

SOB + O2. On oxygen. O2 sat 99% Marked ST segment depression on EKG 59.0 kg Ht 177 cm Computation constant - .547 Swan Ganz inserted. Nitroglycerine infusion started wwwemedicine.com/med/topic2956.c?htm

coronary 1320 Insert 1325 13:29 13:38 1435

CO ST depressed 4.84 HOB 45

CI 2.86

SI

SVRI

PVRI 279

HR 90 92 92

BP 92/69 (78) 94/70 94/57

PAP

(mean)

38/10 RV

(21)

39/18 PAP

(27)

37/21 42/28

(27) (33)

30/20

(24)

PCWP 20 17 22 18

RAP 9 4 6

SvO2

SVR 1041

PVR 165

LVSWI 35.8 21.2

RVSWI 16.46 9.74

Intramural MI ST segment depression in the night BP okay Wedge increased from 14 mm Hg -19 mm Hg Awoke – suddenly SOB – sat bolt upright O2 sats in the 80’s on 100% O2 Nitroglycerine increased to 3 mcg/kg/min Morphine 12 lead done 5:20 am Esmolol 400 mcg/kg/min Tachycardia PAP 55/22 reflecting Marked LV failure

Intramural MI LOC decreased Emergent intubation Systole of 40 mm Hg Epi - .02 mcg/kg/min Vasopressin .0004 units/kg/hr Nitroglycerine 6 mcg/kg/min Bicarb Ca++ Volume 2 units PRBC Troponin and CPK increased Esmolol off V tachycardia

Intramural MI Reimplantation of intramural LCAReimplantation of intramural LCA Good functionGood function LCA origin in middle of L coronary sinusLCA origin in middle of L coronary sinus Abherrent LMCA from tight sinus of aortaAbherrent LMCA from tight sinus of aorta Unroof the LMCA off the ostiumUnroof the LMCA off the ostium Bipass 91 minBipass 91 min XClamp 41 minXClamp 41 min Nitroglygerine 0.5 mcg/kg/minNitroglygerine 0.5 mcg/kg/min MilrinoneMilrinone Tylenol and KetorolacTylenol and Ketorolac EsmololEsmolol Day 2 – Post op ST depression and diastolic dysfunctionDay 2 – Post op ST depression and diastolic dysfunction

Health & Medicine

Hemodynamics advanced orientation, july 2008 - copy