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
X
Page 1
xxx00.#####.ppt 11/12/2019 2:35:26 PM
Disclosures•None
Page 2
xxx00.#####.ppt 11/12/2019 2:35:26 PM
Learning Objectives•Review ventricular function assessment
•Apply technology for the assessment of ventricular function
•Apply principles of hemodynamic assessment of ventricular function
Page 3
xxx00.#####.ppt 11/12/2019 2:35:27 PM
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
Page 5
xxx00.#####.ppt 11/12/2019 2:35:28 PM
Cardiac Performance•Pre load
•After load
•Contractile function
•Heart rhythm
•Ventricular interdependence
Page 6
xxx00.#####.ppt 11/12/2019 2:35:28 PM
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
Page 7
xxx00.#####.ppt 11/12/2019 2:35:28 PM
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
Page 8
xxx00.#####.ppt 11/12/2019 2:35:29 PM
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
Page 9
xxx00.#####.ppt 11/12/2019 2:35:29 PM
Ferguson, CCM 2008
Page 10
xxx00.#####.ppt 11/12/2019 2:35:30 PM
Compared with the LV, the RV demonstrates a heightened sensitivity to afterload changes
Page 11
xxx00.#####.ppt 11/12/2019 2:35:31 PM
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
Page 12
xxx00.#####.ppt 11/12/2019 2:35:31 PM
Smith, API 1992
Page 13
xxx00.#####.ppt 11/12/2019 2:35:32 PM
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
Page 14
xxx00.#####.ppt 11/12/2019 2:35:33 PM
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
Page 15
xxx00.#####.ppt 11/12/2019 2:35:33 PM
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)
Page 16
xxx00.#####.ppt 11/12/2019 2:35:34 PM
Sinus Rhythm•Maintenance of sinus rhythm and AV synchrony is especially important in the presence of RV dysfunction
Page 17
xxx00.#####.ppt 11/12/2019 2:35:34 PM
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
Page 18
xxx00.#####.ppt 11/12/2019 2:35:35 PM
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
Page 19
xxx00.#####.ppt 11/12/2019 2:35:35 PM
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
Page 20
xxx00.#####.ppt 11/12/2019 2:35:36 PM
Evaluation of Right Ventricle•Chest X ray
•Echocardiogram
•Hemodynamic assessment
•Cardiac MRI
•Other studies
Page 21
xxx00.#####.ppt 11/12/2019 2:35:36 PM
Chest X Ray
•Reasonable sensitivity but poor specificity
Page 22
xxx00.#####.ppt 11/12/2019 2:35:37 PM
Echocardiogram
Page 23
xxx00.#####.ppt 11/12/2019 2:35:37 PM
Page 24
xxx00.#####.ppt 11/12/2019 2:35:38 PM
Page 25
xxx00.#####.ppt 11/12/2019 2:35:39 PM
Ferguson, CCM 2008
Page 26
xxx00.#####.ppt 11/12/2019 2:35:39 PM
Page 27
xxx00.#####.ppt 11/12/2019 2:35:40 PM
5mm = 20% RVEF10mm = 30%15mm = 40%20mm = 50%
Page 28
xxx00.#####.ppt 11/12/2019 2:35:40 PM
Page 29
xxx00.#####.ppt 11/12/2019 2:35:41 PM
Volume assessmentCollapsibilityDistensibility
Fergurson, JASE 2008
Page 30
xxx00.#####.ppt 11/12/2019 2:35:42 PM
Page 31
xxx00.#####.ppt 11/12/2019 2:35:42 PM
Smith, API 2006
Page 32
xxx00.#####.ppt 11/12/2019 2:35:43 PM
Myocardial Performance Index
Tei, JASE 2002
Page 33
xxx00.#####.ppt 11/12/2019 2:35:43 PM
Strain Imaging and Speckle Tracking
McDermott, CMR 2008
Cardinal Saturations
Page 35
xxx00.#####.ppt 11/12/2019 2:35:44 PM
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
Page 36
xxx00.#####.ppt 11/12/2019 2:35:45 PM
Oximetric Detection of Shunts in ChildrenChamber sampled Minimum difference Multiple samples
SVC – RA 9% 7%
RA ‐ RV 5% 4%
RV ‐ PA 6% 4%
Page 37
xxx00.#####.ppt 11/12/2019 2:35:45 PM
Hemodynamic Assessment•General rules
•Description of cardinal saturations
•Description of pressure measurements
•Overview of cardiac ouput measurement
•Description of vascular resistance
Page 38
xxx00.#####.ppt 11/12/2019 2:35:46 PM
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
Page 39
xxx00.#####.ppt 11/12/2019 2:35:46 PM
RA Pressure•Increased a Wave
‐Ventricular hypertrophy
‐Atrial hypertrophy
•Increased v Wave‐Dilated RA
‐Large ASD
‐Severe TR
Page 40
xxx00.#####.ppt 11/12/2019 2:35:47 PM
RA wave form
Smith, API 1992
Page 41
xxx00.#####.ppt 11/12/2019 2:35:47 PM
Cannon “a” wave
Carter, JACC 2006
Page 42
xxx00.#####.ppt 11/12/2019 2:35:48 PM
RV Pressure•Normals:
‐15-30 / 5-8 mmHg
•Increased‐PS, PAH, VSD
•Increased RVEDP‐RV Failure
‐Decreased compliance
‐Hypertrophy
Page 43
xxx00.#####.ppt 11/12/2019 2:35:48 PM
RV Pressure Waveform
Smith, API 1992
Page 44
xxx00.#####.ppt 11/12/2019 2:35:49 PM
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
Page 45
xxx00.#####.ppt 11/12/2019 2:35:49 PM
Pressure Measurements Ventricles
Pierre,Circ 2004
Cardiac Output Measurement
Page 47
xxx00.#####.ppt 11/12/2019 2:35:50 PM
Methods of Cardiac Output Measurement
•Fick principle
•Thermodilution
•Dye dilution curves
Vascular Resistance Measurement
Page 49
xxx00.#####.ppt 11/12/2019 2:35:51 PM
Vascular Resistance•Poiseuille’s Law
Page 50
xxx00.#####.ppt 11/12/2019 2:35:51 PM
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
Page 51
xxx00.#####.ppt 11/12/2019 2:35:51 PM
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
Page 52
xxx00.#####.ppt 11/12/2019 2:35:52 PM
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
Page 53
xxx00.#####.ppt 11/12/2019 2:35:52 PM