Phenotype‐Directed Management of Hypertension in Pregnancy

Figure 1. Integration of placental growth factor (PlGF) testing into clinical care of high‐risk pregnant patients: key points.

Figure 2. Nomograms generated by the University of Washington Medical Center team to interpret the maternal hemodynamics. A, Longitudinal changes in cardiac output (mean±1 SD) in normotensive healthy pregnant patients, as estimated by UltraCom method at the University of Washington, Seattle. Blue line=mean cardiac output; red lines=1 SD. B, Relationship between mean arterial pressure and cardiac output. Isometric lines of total peripheral resistance (TPR) are included in order to display all parameters on 1 graph.

Figure 3. Persistent high output state with chronic hypertension and delivery at 37 weeks. Serial hemodynamic assessments demonstrated high cardiac output. Treatment with atenolol at 15 weeks reduced cardiac output toward normal, but in all stages of pregnancy the patient was in a hyperdynamic state. A, Serial cardiac output measurements. B, Relationship between mean arterial pressure and cardiac output with total peripheral resistance (TPR) plotted as isometric lines.

Figure 4. Hemodynamically directed change in antihypertensive medications resulting in a 37‐week delivery in the setting of suspected growth restriction. A, Serial cardiac output measurements. B, Relationship between mean arterial pressure and cardiac output with total peripheral resistance (TPR) plotted as isometric lines.

Figure 5. High resistance state noted at 32 weeks requiring increasing doses of hydralazine with ultimate delivery at 37 weeks. A, Serial cardiac output measurements. B, Relationship between mean arterial pressure and cardiac output with total peripheral resistance (TPR) plotted as isometric lines.

Figure 6. Proposed recommendations for phenotype‐driven clinical care of hypertensive pregnant patients. LMWH indicates low molecular weight heparin; PlGF, placental growth factor; and sFlt1, soluble fms‐like tyrosine kinase.