agitation, and pain FIG 15.9 Approach to treatment based on systolic, diastolic, or combined hypotension is present and taking into consideration specific disease physiology AP, Aortic pressure; CRT, cardiac resynchronization therapy; HIE, hypoxic-ischemic encephalopathy; IDM, infant of a diabetic mother; LV, left ventricle; SIRS, systemic inflammatory response syndrome; SVR, systemic vascular resistance; TnECHO; targeted neonatal echocardiography (McNamara PJ, Weisz DE, Giesinger RE, Jain A Hemodynamics In: Gordon B Avery, MacDonald MG, Seshia MMK, eds Avery's Neonatology: Pathophysiology and Management of the Newborn Philadelphia: Wolters Kluwer; 2016:457–486.) Table 15.4 Systemic Hypertension Pathophysiology: Decreased Left Ventricular Stroke Output (See Fig 15.9) Possible Causes PPHN Septic (cold) shock Cardiogenic shock Therapeutic Approach (Mechanism) Reduced PVR (e.g., iNO, milrinone [may increase inotropy]) Improve atrial filling pressure (preload) (e.g., fluid bolus, vasopressin [may decrease PVR]) Enhance myocardial systolic performance (e.g., dobutamine, epinephrine) Consider PGE2 infusion if RV dysfunction and DA closed or restrictive Improve myocardial systolic performance (e.g., dobutamine, epinephrine [may increase preload]) Optimize treatment of sepsis Check heart rhythm (rule out arrhythmia) Improve myocardial systolic performance (e.g., dobutamine, epinephrine) DA, Ductus arteriosus; iNO, inhaled nitric oxide; PGE2, prostaglandin E2, PPHN, persistent pulmonary hypertension; PVR, pulmonary vascular resistance; RV, right ventricle Table 15.5 Systemic Hypertension Pathophysiology: Decreased Systemic Vascular Resistance (See Fig 15.9) Possible Causes Systemic hypovolemia Warm shock PDA Therapeutic Approach (Mechanism) Optimize filling pressures (preload)-fluid boluses (max 2 of 10 mL/kg each) ± colloid Increase SVR once adequate volume given (e.g., vasopressin, dopamine) Optimize filling pressures (preload)-fluid boluses (max 2 of 10 mL/kg each) Increase SVR (e.g., dopamine, norepinephrine, vasopressin [may increase atrial filling pressure]) Ductal closure strategies (NSAIDs, acetaminophen, surgery) Flow limitation strategies (e.g., permissive hypercapnia, increased PEEP) Enhance LV systolic function (e.g., dobutamine) LV, Left ventricle; NSAID, nonsteroidal antiinflammatory drug; PDA, patent ductus arteriosus; PEEP, positive end-expiratory pressure; SVR, systemic vascular resistance Table 15.6 Systemic Hypertension Pathophysiology: Cardiac Systolic Dysfunction (See Fig 15.9) Cause Physiology Therapeutic Approach (Mechanism) PROGRESSION OF SEVERITY AFTER AN INITIAL PERIOD OF LOW SYSTOLIC ATRIAL PRESSURE PPHN LV dysfunction and/or loss Improve atrial filling pressure (preload) of vascular tone (e.g., fluid bolus, vasopressin [unless LV dysfunction on TnECHO]) Enhance myocardial systolic performance (e.g., dobutamine, epinephrine) Cardiogenic shock Worsening LV function (? Enhance myocardial systolic performance impending arrest) (e.g., dobutamine, epinephrine) PROGRESSION OF SEVERITY AFTER AN INITIAL PERIOD OF LOW DIASTOLIC ATRIAL PRESSURE Hypovolemia or warm shock Myocardium unable to Optimize filling pressures (preload)compensate or progression fluid boluses (max 2 of 10 mL/kg each) to cardiac dysfunction Increase SVR (e.g., dopamine, norepinephrine, vasopressin [if no LV dysfunction]) PDA Large-volume shunt and Flow limitation strategies (e.g., myocardium unable to permissive hypercapnia, increased compensate PEEP) Enhance LV systolic function (e.g., dobutamine, dopamine [if critical DAP]) BOTH SYSTOLIC AND DIASTOLIC PRESSURE LOW AT PRESENTATION (PROFOUND HYPOTENSION) Manage as severe warm shock with LV As above + early hydrocortisone dysfunction if no echo available (rule out adrenal insufficiency) DAP, Diastolic atrial pressure; LV, left ventricle; PDA, patent ductus arteriosus; PEEP, positive end-expiratory pressure; PPHN, persistent pulmonary hypertension; SVR, systemic vascular resistance; TnECHO; targeted neonatal echocardiography FIG 15.10 Factors governing cellular metabolism and the adequacy of tissue oxygenation subdivided according to tissue oxygen delivery and consumption BP, Blood pressure; SVR, systemic vascular resistance Volume There have been no studies of volume versus no treatment The systematic review of trials of early expansion found no evidence of benefit,189 and bench research suggests no benefit to administering volume to hypotensive animals that are not hypovolemic.190 Trials comparing normal saline with albumin found no advantage of either therapy in reducing mortality or improving cardiovascular outcomes and albumin is associated with a greater risk of impaired gas exchange.191,192 Volume should be restricted to treating hypovolemia where there is an identified precipitating factor, such as acute loss of blood Vasopressor Agents Dopamine is a sympathetic amine and the most commonly used vasoactive agent in the neonatal intensive care unit It has mixed β-1 and α-adrenergic effects