What is the clinical significance of derived values such as Cardiac Vascular System (CVS) performance, Stroke Volume (SV), Systemic Vascular Resistance (SVR), Left Ventricular Stroke Work (LVSW), SVR Index (SVRI), Pulmonary Vascular Resistance (PVR), and Pulmonary Vascular Resistance Index (PVRI) in cardiac anesthesia?

Clinical Significance of Derived Hemodynamic Values in Cardiac Anesthesia

Stroke Volume (SV) and Cardiac Index (CI)

Stroke volume and cardiac index are fundamental determinants of tissue oxygen delivery and must be continuously monitored during cardiac anesthesia to guide fluid resuscitation, inotropic support, and vasopressor therapy. 1

• SV represents the volume of blood ejected per heartbeat and directly reflects ventricular contractility, preload, and afterload interactions 2
• CI (cardiac output divided by body surface area) provides size-adjusted assessment allowing standardized comparisons across patients of different body sizes 1
• During cardiac surgery, SV typically increases with volume loading in preload-responsive patients, while decreased SV may indicate hypovolemia, myocardial dysfunction, or excessive afterload 3
• Continuous SV monitoring via arterial pulse contour analysis enables real-time assessment of hemodynamic interventions, though recalibration is required when systemic vascular resistance changes significantly 4

Clinical Applications of SV Monitoring

• Stroke volume variation (SVV) during mechanical ventilation predicts fluid responsiveness in cardiac surgical patients, with baseline SVV correlating significantly with volume-induced changes in stroke volume index (r² = 0.66) 4
• SVV >10-13% typically indicates preload responsiveness in mechanically ventilated patients without arrhythmias or spontaneous breathing efforts 3, 4
• Dynamic SV assessment is superior to static pressure measurements (CVP, PCWP) for guiding fluid therapy, as static parameters are insensitive indicators of volume status 5

Common Pitfalls with SV Monitoring

• Pulse contour-derived SV becomes inaccurate during rapid changes in vascular tone, requiring recalibration with transpulmonary thermodilution 4
• SVV loses predictive value in spontaneously breathing patients, as demonstrated by lack of correlation (r = 0.19) between baseline SVV and stroke volume changes in normoventilated patients 6
• Arrhythmias, open chest conditions, and right ventricular dysfunction invalidate SVV interpretation 3

Systemic Vascular Resistance (SVR) and SVR Index (SVRI)

SVR represents the afterload against which the left ventricle must eject and is calculated as (MAP - RAP)/CO × 80, with normal values of 800-1200 dynes·s·cm⁻⁵. 1

• SVRI adjusts SVR for body surface area (normal ~2000-2400 dynes·s·cm⁻⁵·m²), providing standardized assessment across different patient sizes 1
• Low SVR state (SVRI <1800 dynes·s·cm⁻⁵·m²) occurs in 44% of patients after cardiopulmonary bypass, representing systemic inflammatory response syndrome 7
• SVR typically demonstrates inverse relationship with cardiac output—as CO increases, SVR decreases through compensatory vasodilation 8

Clinical Significance During Cardiac Surgery

• Post-bypass low SVR manifests as sustained increase in cardiac index and CVP preceding the decrease in mean arterial pressure, with maximal hypotension occurring at 8 hours postoperatively 7
• Patients with low SVR respond better to vasopressors than volume loading, as further increasing cardiac index through fluid administration is counterproductive 7
• Male gender, longer cross-clamp times, and lower postoperative platelet counts predict development of low SVR state 7
• SVR monitoring guides vasopressor vs. inotrope selection—low SVR with adequate CO requires vasopressors (phenylephrine, norepinephrine), while high SVR with low CO requires afterload reduction 1

Critical Relationship with Pulmonary Vascular Resistance

In pulmonary arterial hypertension, SVR must exceed PVR to prevent right ventricular ischemia, as right ventricular coronary perfusion occurs during both systole and diastole. 1

• If systolic pulmonary arterial pressure exceeds systolic systemic arterial pressure (PVR > SVR during systole), right ventricular ischemia results 1
• This principle guides vasopressor management in patients with pulmonary hypertension undergoing cardiac surgery 1

Left Ventricular Stroke Work (LVSW) and LVSW Index (LVSWI)

LVSW quantifies the external work performed by the left ventricle per beat, integrating both pressure generation and volume ejection to assess ventricular contractile efficiency.

• LVSW is calculated as SV × (MAP - PCWP) × 0.0136, with normal values approximately 60-80 gram-meters per beat
• LVSWI adjusts for body surface area (normal 50-62 gram-meters/m²/beat), providing size-independent assessment of ventricular performance
• LVSW reflects the interaction between contractility, preload, and afterload, making it a comprehensive index of left ventricular function
• Decreased LVSW indicates either reduced contractility or inadequate preload, while increased LVSW may represent compensatory response to increased afterload or enhanced inotropy

Clinical Applications in Cardiac Anesthesia

• LVSW monitoring helps differentiate between primary myocardial dysfunction and loading condition abnormalities during hemodynamic instability
• Serial LVSW measurements guide inotropic therapy titration, with increasing LVSW indicating positive response to inotropes
• LVSW decreases during myocardial ischemia before changes in ejection fraction become apparent, providing early warning of inadequate myocardial oxygen supply
• Comparison of right and left ventricular stroke work indices helps identify ventricular-specific dysfunction in complex cardiac surgical cases

Pulmonary Vascular Resistance (PVR) and PVR Index (PVRI)

PVR is calculated as (mPAP - PCWP)/CO, with normal values <2-3 Wood units, and represents the afterload against which the right ventricle must eject. 1

• PVR >3 Wood units defines precapillary pulmonary hypertension according to 2018 guidelines, though 2024 guidelines use >2 Wood units as the threshold 1
• PVRI (measured in Wood units·m²) adjusts PVR for body surface area, which is particularly important in pediatric populations where body size varies significantly 1
• Direct measurement via right heart catheterization is mandatory for accurate PVR calculation, as echocardiographic estimation has limited positive predictive value (25-64%) 1

Critical Clinical Thresholds in Cardiac Surgery

PVR >2.5 Wood units or PVRI >4 Wood units·m² represents a contraindication for congenital heart disease shunt closure. 1

• PVRI >6 Wood units·m² predicts poor prognosis in children with congenital heart disease undergoing cavopulmonary surgery, regardless of lung morphology 1
• Transpulmonary gradient (mPAP - PCWP) >6 mmHg suggests high risk for poor outcomes in cavopulmonary anastomosis 1
• PVRI <7-8 Wood units·m² in response to vasodilator challenge predicts good surgical outcomes in patients with simple shunts 1
• Many centers use preoperative PVR <10-14 Wood units and pulmonary/systemic resistance ratio ≤2/3 as thresholds for acceptable surgical risk 1

Measurement Considerations and Pitfalls

• PCWP must be measured at end-expiration during spontaneous breathing to ensure accuracy, with the external pressure transducer zeroed at the mid-thoracic line 1
• Blood pH profoundly affects pulmonary vascular tone—acidosis causes vasoconstriction while alkalosis causes vasodilation, making arterial blood gas awareness critical during catheterization 1
• General anesthesia lowers systemic arterial blood pressure, affecting resistance calculations and requiring standardized measurement conditions 1
• In single-ventricle patients after bidirectional Glenn operation, PCWP may underestimate true PVR 1
• Tricuspid regurgitation and right ventricular dilatation cause erroneous cardiac output measurements by thermodilution, affecting all derived resistance calculations 1

Intraoperative PVR Management

• Maintain adequate oxygenation and avoid hypercapnia, as both hypoxemia and respiratory acidosis increase PVR
• Optimize ventilation strategies—high PEEP increases PVR through alveolar compression, while atelectasis increases PVR through hypoxic vasoconstriction
• Consider inhaled pulmonary vasodilators (nitric oxide, epoprostenol) when PVR elevation threatens right ventricular function
• Avoid systemic hypotension, as decreased coronary perfusion pressure combined with elevated right ventricular afterload precipitates right ventricular ischemia 2

Integration of Derived Values for Clinical Decision-Making

Simultaneous assessment of SV, SVR, PVR, and LVSW provides comprehensive hemodynamic profiling that guides specific therapeutic interventions during cardiac anesthesia.

• Low CO with high SVR and normal LVSW: Consider afterload reduction with vasodilators
• Low CO with low SVR and decreased LVSW: Indicates primary myocardial dysfunction requiring inotropic support
• Low CO with high PVR and normal left-sided parameters: Suggests isolated right ventricular dysfunction requiring pulmonary vasodilators and right ventricular-specific inotropes
• High CO with low SVR: Represents vasodilatory shock requiring vasopressor therapy rather than volume loading 7

Monitoring Strategy During Cardiac Surgery

• Establish invasive arterial and central venous access before induction for continuous pressure monitoring 9
• Consider pulmonary artery catheterization in high-risk patients (severe pulmonary hypertension, right ventricular dysfunction, complex congenital heart disease) to enable direct PVR calculation 1
• Implement pulse contour cardiac output monitoring for continuous SV and SVR assessment, with periodic recalibration during hemodynamic instability 4
• Utilize transesophageal echocardiography for real-time assessment of ventricular function, volume status, and regional wall motion abnormalities 5
• Measure derived values at standardized time points: post-induction, post-sternotomy, during bypass, post-bypass, and after sternal closure 8