How is systemic vascular resistance (SVR) managed in the Cardiovascular Intensive Care Unit (CVICU)?

Management of Systemic Vascular Resistance in the CVICU

Systemic vascular resistance (SVR) management in the Cardiovascular Intensive Care Unit (CVICU) requires careful assessment and targeted interventions to maintain optimal hemodynamic balance, with the primary goal of maintaining SVR higher than pulmonary vascular resistance (PVR) to ensure adequate right ventricular coronary perfusion and prevent right ventricular ischemia.

Assessment of SVR

• SVR is calculated as (mean arterial pressure minus right atrial pressure) divided by cardiac output, typically measured in dynes/s/cm² 1
• Direct measurement via pulmonary artery catheter provides the most accurate assessment of SVR in critically ill patients 1
• Central venous pressure monitoring helps detect and guide treatment of abnormal SVR 1
• Clinical signs of increased SVR include absent or weak distal pulses, cool extremities, prolonged capillary refill, and narrow pulse pressure with relatively increased diastolic blood pressure 2
• Clinical assessment alone has poor correlation with objective measurements, with one study showing only 45.9% agreement between physician assessment and ultrasonic cardiac output monitor measurements 3

Management of Low SVR States

• Low SVR states are common in post-cardiopulmonary bypass patients (44% in one study) and are associated with significant mortality 4
• Vasopressors are the first-line treatment for hypotension due to low SVR to restore vascular tone 4
• Norepinephrine is recommended for maintaining mean arterial pressure in hyperdynamic states, which has been shown to improve urine output and creatinine clearance 2
• Vasopressin at replacement doses can effectively offset the potential drop in SVR when using inotropes like dobutamine or milrinone 2
• In septic patients with low SVR, maintaining a cardiac index between 3.3 and 6.0 L/min/m² is associated with best outcomes 2
• Extremely low SVR (below 450 dynes × s/cm⁵) is associated with significantly higher mortality regardless of etiology and requires aggressive intervention 5

Management of High SVR States

• Vasodilator therapy with additional volume loading is the effective approach for patients with high SVR 2
• Nitroprusside is effective for high-afterload left ventricular failure due to its potent arterial and venous dilation properties 2, 6
• Nitroglycerin can be used for vasodilation but has more pronounced effects on venous than arterial circulation 7, 6
• Phosphodiesterase inhibitors (milrinone) or α-adrenergic blockers (phenoxybenzamine, phentolamine) are effective for reducing SVR in patients with single-ventricle physiology 2
• For patients with high SVR and normal blood pressure but low cardiac output, vasodilator therapies should be given in addition to inotropes 2

Special Considerations in CVICU

Right Ventricular Failure

• Maintain SVR greater than PVR to ensure adequate right ventricular coronary perfusion 2
• Right ventricular coronary perfusion occurs during both systole and diastole, so if PVR exceeds SVR (systolic pulmonary arterial pressure > systolic systemic arterial pressure), right ventricular ischemia can result 2
• Systolic systemic arterial pressure goals are typically higher in pulmonary hypertension patients than in non-pulmonary hypertension patients 2

Inotrope and Vasopressor Selection

• Inotropes with neutral or beneficial effects on PVR include dobutamine, milrinone, and epinephrine 2
• Dobutamine is often preferred over milrinone due to its shorter half-life when there's risk of hypotension 2
• Vasopressin is particularly useful in septic or liver pulmonary hypertension patients, in whom vasopressin-deficiency is common 2

Pulmonary Hypertension

• Inhaled nitric oxide can acutely decrease PVR and improve cardiac output without affecting SVR, making it valuable in managing right ventricular failure 2
• Intravenous or inhaled pulmonary vasodilators can reduce right ventricular afterload for pulmonary arterial hypertension and right ventricular failure 2
• Minimizing intrathoracic positive pressure ventilation, correcting acidosis, and improving hypoxic pulmonary vasoconstriction may improve left ventricular filling in right ventricular failure 2

Single-Ventricle Physiology

• In patients with single-ventricle physiology, the balance between pulmonary and systemic blood flow is controlled by the relative resistances in the pulmonary and systemic vascular beds 2
• High inspired oxygen concentration can dilate the pulmonary vascular bed and decrease pulmonary vascular resistance, increasing pulmonary blood flow at the expense of systemic blood flow 2
• To increase systemic blood flow and reduce pulmonary overcirculation, reduce factors that decrease pulmonary vascular resistance and reduce SVR with phosphodiesterase inhibitors or α-adrenergic blockers 2

Monitoring and Titration

• Continuous monitoring of physiologic parameters (blood pressure, heart rate, and other measurements such as pulmonary capillary wedge pressure) is essential to achieve the correct dose of vasoactive medications 2
• Cardiac index between 3.3 and 6.0 L/min/m² is associated with best outcomes in septic shock patients compared with patients without septic shock for whom a cardiac index above 2.0 L/min/m² is sufficient 2
• In patients with increased intra-abdominal pressure (>12 mmHg), therapeutic reduction using diuretics and/or peritoneal drainage may be necessary to restore perfusion pressure 2
• Careful monitoring of the shock index (heart rate/systolic blood pressure) can help assess the effectiveness of interventions 2

Pitfalls and Caveats

• Volume status assessment in pulmonary hypertension patients is notoriously difficult, and non-invasive estimates of central venous pressures may be misleading 2
• The traditional belief that the right ventricle is preload dependent often leads to inappropriate and detrimental volume loading in right ventricular dysfunction 2
• The right ventricle prefers euvolemia with a central venous pressure of 8-12 mmHg 2
• Right ventricular distention causes leftward interventricular septal shift, compromising left ventricular filling and reducing cardiac output 2
• Exercise-induced sympatholytic vasodilation in skeletal muscle may significantly exacerbate systemic arterial hypotension in acute shock states and resuscitation scenarios 8
• At least a quarter of patients with hypotension and low SVR have non-septic etiologies with similar mortality to septic patients 5