How to Best Monitor Right X and Left Ventricular Function · 2019-11-21 · How to Best Monitor...

How to Best Monitor Right and Left Ventricular Function

Saul Flores, MD, FAAP, FACCCardiac Intensivist and CardiologistTexas Children’s Hospital/Baylor College of MedicinePediatric Critical Care Summit of the Americas11/09/19

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Disclosures•None

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Learning Objectives•Review ventricular function assessment

•Apply technology for the assessment of ventricular function

•Apply principles of hemodynamic assessment of ventricular function

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Sample Case•14 year old teenager comes to the ED with severe respiratory distress. Describes symptoms for las 7 days that worsened overnight. Patient has had a runny nose and also noticed that ”whole” body appears swollen. Initial vital signs demonstrate HR 130 bpm, RR 35 bpm, BP 88/35 48, O2Sat 93% on RA and temp 102 F. Initial CXR demonstrates diffuse bl alveolar infiltrates and cardiomegaly.

•What is the best next step in the management of this patient?

Physiological Assessment of the Right Ventricle

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Cardiac Performance•Pre load

•After load

•Contractile function

•Heart rhythm

•Ventricular interdependence

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Pre Load•Filling of RV

‐ RV filling normally starts before and finishes after LV

‐ RV isovolumic relaxation time is shorter

‐ RV filling velocities (E and A) and the E/A ratio are lower

•RV can accommodate varying degrees of pre load while maintaining a stable cardiac output and normal filling pressures

•Two characteristics of RV:‐ Distensibility of its free wall

‐ Compliance-the ability to increase volume without significant changes in the wall surface area

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Pre Load/Filling of RV•Dilation of the RV caused by volume overload is usually well tolerated

•However, two consequences lead to symptoms:‐Functional tricuspid regurgitation

‐Compression of LV by mechanism of ventricular interdependence – decreased cardiac output

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After Load•Normal after load is minimal – low impedance, highly distensible pulmonary vascular system

•PVR is the most commonly used index of afterload, but may not reflect the complex nature of ventricular afterload

•Several factors modulate PVR, including:‐ Hypoxia

‐ Hypercarbia

‐ Cardiac output

‐ Pulmonary volume and pressure

‐ Specific molecular pathways: Nitric oxide, prostaglandin, endothelin

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Ferguson, CCM 2008

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Compared with the LV, the RV demonstrates a heightened sensitivity to afterload changes

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RV Contraction•RV consist of:

‐ The superficial oblique myocardial fibers, in continuity with the LV fibers

‐ Deeper layer of longitudinally arranged

•LV has additional middle transverse fibers

•RV contraction begins at the inflow region and progresses toward the outflow tract (likened to a bellows)

•In distinction, the LV contracts by squeezing motion (likened a wringing a towel) from the LV apex to the outflow tract

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Smith, API 1992

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RV Pressure Volume Loop

• External mechanical work is lower in the RV

• RV pressure begins to decline before closure of the pulmonic valve- RV continues to eject blood because of high compliance and low resistance of the pulmonary vasculature

Dell’Italia, CCM 2002

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RV Elastance

• Maximal RV elastance better reflects RV contractility than does the end-systolic elastance

• The normal maximal RV elastance is 1.3 +/-0.84 mmHg

Dell’Italia, CCM 2002

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RV Pressure Tracing•RV pressure are lower than LV pressures

•Show early peaking and a rapidly decline in contrast to the rounded contour of LV pressure tracing

•RV isovolumic contraction time is shorter because RV systolic pressure rapidly exceeds the low pulmonary artery diastolic pressure

•End-systolic flow may continue in the presence of a negative ventricular-arterial pressure gradient (hangout interval)

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Sinus Rhythm•Maintenance of sinus rhythm and AV synchrony is especially important in the presence of RV dysfunction

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Ventricular Interdependence• The size, shape, and compliance of a ventricle may affect size, shape, and pressure-volume relationship of the other ventricle through direct mechanical interaction

• Systolic – mainly through the interventicular septum & continuity of muscle fibers

• Diastolic – mainly through the pericardium

Smith, API 2008

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Acute RV pressure or volume overload states

Dilation of the RV

Shift of IVS towards LV

Alter LV geometry & increases pericardial constraint

LV diastolic pressure-volume curve shifts upward (decrease distensibility), decreased LV preload, an increased LV end-

diastolic pressure

Low cardiac output

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Summary•Thin walled, more complaint, higher ED volumes

•Equal cardiac output at less energy expenditure

•Ejects equal amount of blood at lower RVEF

•Tolerates volume overload better

•More efficient work output

•Pre load and after load sensitive

•Ventricular interdependence

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Evaluation of Right Ventricle•Chest X ray

•Echocardiogram

•Hemodynamic assessment

•Cardiac MRI

•Other studies

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Chest X Ray

•Reasonable sensitivity but poor specificity

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Echocardiogram

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Ferguson, CCM 2008

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5mm = 20% RVEF10mm = 30%15mm = 40%20mm = 50%

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Volume assessmentCollapsibilityDistensibility

Fergurson, JASE 2008

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Smith, API 2006

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Myocardial Performance Index

Tei, JASE 2002

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Strain Imaging and Speckle Tracking

McDermott, CMR 2008

Cardinal Saturations

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Cardinal Saturations•Pulmonary arterial = 67-86% mean 77%

•Pulmonary venous = >95%

•Systemic Arterial = >95%, except IAA, TGA + PAH

•Systemic venous = Used to infer potential shunting

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Oximetric Detection of Shunts in ChildrenChamber sampled Minimum difference Multiple samples

SVC – RA 9% 7%

RA ‐ RV 5% 4%

RV ‐ PA 6% 4%

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Hemodynamic Assessment•General rules

•Description of cardinal saturations

•Description of pressure measurements

•Overview of cardiac ouput measurement

•Description of vascular resistance

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RA Pressure•Normals:

‐ a, c, v Waves

‐ a wave < 8 mmHg

‐ v wave < 7 mmHg

‐ Mean < 6 mmHg

•a wave = atrial systole; first wave after P

•c wave = early V systole transmitted through AV valve

•v wave – end of systole – continued atrial filling against closed TV

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RA Pressure•Increased a Wave

‐Ventricular hypertrophy

‐Atrial hypertrophy

•Increased v Wave‐Dilated RA

‐Large ASD

‐Severe TR

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RA wave form

Smith, API 1992

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Cannon “a” wave

Carter, JACC 2006

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RV Pressure•Normals:

‐15-30 / 5-8 mmHg

•Increased‐PS, PAH, VSD

•Increased RVEDP‐RV Failure

‐Decreased compliance

‐Hypertrophy

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RV Pressure Waveform

Smith, API 1992

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Pulmonary Pressures•Normals:

‐ 15-25 / 8-12 mmHg

• Increased ‐ L -> R shunt

•VSD, PDA

‐ Pulmonary venous return resistance

•Obstructed veins: congenital or post-op

•Mitral disease: stenosis or severe regurgitation

•Elevated LVEDP

‐ Thromboemboli

•PVOD -> Eisenmenger physiology

•Primary pulmonary hypertension

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Pressure Measurements Ventricles

Pierre,Circ 2004

Cardiac Output Measurement

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Methods of Cardiac Output Measurement

•Fick principle

•Thermodilution

•Dye dilution curves

Vascular Resistance Measurement

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Vascular Resistance•Poiseuille’s Law

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Resistance•Resistance = Drop in pressure across a vascular bed/Volume of blood flowing through the vessels

•Vascular Resistance = Mean arterial – mean venous pressure/Flow

•PVR = Mean PAP – Mean PVP/Qp

•Wood unit = mmHg/L/min = mmHg x min/L

•Indexed for BSA = Wood U x m2

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Pulmonary Vascular Resistance•Rp = Mean PA - Mean PV / Qp

•Normal PVR:‐First week life = 8-10 U x m2

‐ Infants and children = 1-3 U x m2

•Measurement unreliable if:‐Discontinuous or stenotic PA’s

‐Ao-PA shunt: differential flow to each lung

‐Multiple sources of Qp with different O2 sats

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Summary•The importance of clear understanding of ventricular mechanics

•Exposure to current and novel technologies for ventricular function assessment

•Clear hemodynamic assessment of ventricular function

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How to Best Monitor Right X and Left Ventricular Function · 2019-11-21 · How to Best Monitor...

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