Right Ventricle. Interaction with the pulmonary circulation. Fellowship Intensive Care Nijmegen
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1 Right Ventricle Interaction with the pulmonary circulation Fellowship Intensive Care Nijmegen
2 Normal right ventricle PAP 25/10 EF 62 ± 8% Constant low pressure perfusion of the lung Maintain low RA pressure SVI 43 ± 13 ml/m 2 EDVI 64 ± 13 ml/m 2 End-Diastole 2-3 mm Under normal circumstances the RV is not essential for an adequate CO
3 Venous return MSFP Fluid challenge Venous resistance VR = MSFP - RAP Venous resistance 0 mm Hg 1,8 1,6 1,4 1,2 1 0,8 0,6 0,4 0,2 0 Before After MSFP Pressure gradient and resistance match metabolic demand Cecconi M. Intensive Care Med 2013;39:
4 Intrathoracic pressure ABP (mmhg) SVI (ml/m2) Time (s) ABP SVI Pressure (mmhg) Time (s) CVP Ppc Paw Ppl
5 RV preload Stroke work (g.m) Mean atrial pressure (cm H2O)
6 Changes P ra and P pericardium after fluid loading Cardiac surgery N = 9 FC van 2.1 L Pra (mmhg) Pra = 0.99 Ppericard Ppericardium (mmhg) Tyberg JV. Circulation 1986;3:
7 EDV ESV ml PEEP (cm H2O) No relationship between RVEDV en RVEDPtm Pinsky MR. Am Rev Respir Dis 1992;146:
8 RV EDV and RV ESV Lineair with normal slope 0.7 (EDV/ESV = 0.7) Unexpected - higher EDV should result in higher EF and therefore relatively lower ESV Pinsky MR. Am Rev Respir Dis 1992;146:
9 Absolute end-diastolic RV pressure More a function of pericardial restraint/pericardial pressure/itp than RV-end diastolic stretch
10 Conclusion (1) Normal RV fills below stressed volume (wall stretch) CVP means a hypertrophied RV with diastolic dysfunction or over distended
11 RV contractility Primarily by longitudinal shortening Peristaltic fashion Inflow track mid-wall outflow track Timing difference ms RV contraction
12 Ees Contractility
13 Different for RV More than half of RV developed pressure comes from LV free wall contraction Explains why LVAD insertion in patient with combined LV failure and mild PH may induce RV failure
14 RV afterload Wall tension of RV Under normal conditions RV afterload dependent on: Distribution of blood flow in the lung Degree of hyperinflation Active increase in pulmonary vasomotor tone
15 Other effect of lung inflation Compression of the cardiac fossa Effect similar to cardiac tamponade
16 Consequences MSFP should equally increase otherwise CO falls Increased afterload RAP Impaired contractility If fluid resuscitation increases RAP patient is probably not fluid responsive
17 Ventriculo-arterial coupling Pulmonary vascular tone RV contractility Expressed as Ea/Ees ratio = total of resistance/compliance/impedance : contractility For the left ventricle optimal E/Ees = 0.5-1
18 Changes in pulmonary Ea A. Effect of Changing E a Right Ventricular Pressure (mmhg) 60 E a Increased E a Decreased E a Constant E es V o RV Volume EDV
19 Changes in RV contractility B.Effect of Changing E es 60 Increased E es Right Ventricular Pressure (mmhg) E a Decreased E es Constant E a V o RV Volume EDV
20 Changes in RV preload C.Effect of Changing Preload for a Constant E es and E a 60 E es Right Ventricular Pressure (mmhg) E a Fig. 1 V o RV Volume EDV
21 Pulmonary hypertension Pulmonary Arterial Pressure (mmhg) A. Calculation of Pmax B. Calculation Ees/Ea coupling Measured Ppa values Calculated Ppa max Time (msec) Pulmonary Arterial Pressure (mmhg ) PAH: Ees/Ea=1 Ees=3 Ea=3 Ea=0.5 P max Ees=1 P max Right Ventricular Volume (ml) Normal: Ees/Ea=2
22 Acute pulmonary hypertension Decreased CO and BP RV dilatation Septal shift Reduced LV compliance RV ischemia Reduced coronary blood flow
23 Central venous pressure Single static measurement does not predict blood volume or fluid responsiveness Trends in CVP combined with indicators of cardiac output are especially useful for fluid management Waveform analysis may also give valuable information (fluid responsiveness, inspiratory effort, chest wall compliance tricuspid valve competence, RV compliance, tamponade)
24 CVP determined by CO and VR Cardiac Function Return Function L Q R Rv MSFP Q Q Q MSFP Pra Pra
25 Three ways to increase CVP A Q B Q C Q Pra Pra Pra Cardiac function Stressed volume Venous resistance
26 Measurement of CVP sternum; this point is called the sternal angle and is identified on clinical examination by a slight protuberance due to the angle formed by the articulation of the manubrium and sternum. On average, the midpoint of the right atrium is 5 cm vertically below the sternal angle. This is true whether a person lies flat or sits up at a 60! angle, because the right atrium is a relatively round structure and is just below the sternum.13 The center of the right atrium thus remains directly below the sternal angle when the torso is rotated upward. Bedside measurement of CVP gives a value in centimeters of water. This can be converted to millimeters of mercury by dividing the value in centimeters of water by This is based on the density of mercury, which is 13.6 times that of water, and conversion from centimeters to millimeters. When assessing jugular venous distention, the measurement should be made at the base of the pulsations seen in the neck rather than at the top of the pulsations, for this value is closest to the value obtained from the pressure waves on monitors. CVP can also be determined with a simple fluid column inserted into a central vessel and similarly by the column of fluid filling a central line, but one must guard against allowing air to be sucked in through the system. These values are closer to the mean value on electronic monitors. Ultrasonography can also be used to measure CVP noninvasively14,15 by assessing the level of collapse in the jugular veins, which is like looking at the top of the column. Three things must be considered when taking pressure measurements with fluid-filled catheters: zeroing, calibrating, and leveling. All pressures are measured relative to a reference value. The standard reference value or zero is atmospheric pressure, because this is this represents the location at which blood comes back to the heart and is the level from which blood is pumped out again (Fig 3). As indicated earlier for assessment of jugular venous distention on physical examination, the sternal angle is a good reference point because it is 5 cm vertically above the mid-right atrium, and this reference level can also be used to level transducers. This is done by placing a carpenter s leveling device on the sternal angle and setting the transducer 5 cm below it. However, most centers use the midaxillary line at the fourth interspace for the reference level, because a measuring device is not required, and this approach is more adaptable in the operating room (Fig 3). The proper level to use on the transducer is the level at which the stopcock can be opened to air, for this is the condition that was used to zero the system and accounts for the Optimal A
27 Measurement of CVP End-expiratory measurement unless active expiration
28 S wave of QRS
29 Clinical use of CVP Clinical reasoning Lage RR Lage CO CVD 0 Unlikely Tamponade PE RV failure unless: GI bleeding Excessive diuresis Sepsis Lage RR Lage CO CVD Unlikely Hypovolemia unless: High Ppl RV failure
30 Clinical use of CVP It is unlikely that a patient with a CVP > 10 mmhg will respond to a fluid challenge ( 15%) Patients that may respond have longstanding pulmonary HT with thickened right ventricular wall, high pleural pressure, cardiac tamponade or restrictive cardiac disease
31 Clinical use of CVP CVP CO Implication Example Increased cardiac function Decreased cardiac function Increased return function Decreased return function Increase in both functions Decrease in both functions HR, contractility, afterload Caution: PP Stressed vascular volume or venous resistance
32 RV dysfunction in ARDS Often defined as RV dilatation with or without septal dyskinesia TAPSE < 17 mm, pulsed Doppler S wave < 9.5 cm/s, RV fractional area change < 35% and RV EF < 45% Reported incidence 22-50% and associated with increased morbidity and mortality
33 Risk for RV dysfunction Pneumonia as the underlying cause Driving pressure 18 cmh2o P/F < 100 mmhg PaCO2 > 48 mmhg Risk for acute cor pulmonale (%) points 3 points 4 points Higher mortality with acute cor pulmonale (45 vs 25%) Mekontso-Desap A. Intensive Care Med 2016
34 Pathphysiology Imbalance between vasoconstrictors/vasodilators (sepsis) Endothelial injury with in situ thrombosis Hypoxic pulmonary vasoconstriction Hypercapnia and acidemia Muscularization of nonvascular arteries High tidal volume ventilation and PEEP
35 Extra-alveolar blood vessels Alveolar blood vessels Pulmonary vascular resistance Total vascular resistance Alveolar blood vessels Extra-alveolar blood vessels RV FRC TLC
36 Treatment Optimization of RV preload discussed in detail RV failure Increasing RV contractility discussed in detail RV failure Reducing RV afterload discussed in detail RV failure Right ventricle-protective ventilation strategies (+ prone) Considers ECLS / ECCO2R as rescue therapies
37 IAP PaO2 Recruitment VR Central BV PVR RV preload RV afterload LV preload No CO increase No Preload reserve Yes CO increase Jozwiak M. Am J Respir Crit Care Med 2013;188:
38 Prone position and RV failure Before PP After 18 h of PP P-value SAP (mm Hg) 115 ± ± 14 NS HR (bpm) 107 ± ± 13 0,019 CI (l/min/m 2 ) 2.9 ± ± 0.8 0,013 RVEDA/LVEDA 0.91 ± ± 0.21 < 0,001 Septal eccentricity 1.5 ± ± 0.1 < 0,001 TR (n) 20 7 LVEDV (ml) 45 ± ± 21 < 0,001 LVEF (%) 58 ± ± 9 NS N = 21 Severe ARDS with PF < 100 Veillard-Baron A. Chest 2007;132:
39
40 VV-ECMO N = 13 Reis Miranda D. Am J Respir Crit Care Med 2015;191:
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