Version May 2024
| Lesions | Hemodynamic goals | Avoid | Intervention if needed | Physiologic concepts |
| Right-to-left shunting | Maintain or increase SVR | Avoid systemic vasodilation Avoid increases in PVR | Administer a vasoconstrictor (vasopressin is preferred over phenylephrine because vasopressin increases SVR without increasing PVR). Avoid or treat hypoxia or hypercarbia. | Peripheral vasodilation decreases LVEDP and LAP, leading to an increase in right-to-left shunting and a decrease in SpO2 and cyanosis. An increase in PVR will increase right-sided pressures and also increase right-to-left shunting. Because vasopressin increases SVR without increasing PVR, it is preferable to use vasopressin rather than phenylephrine to increase SVR. |
| Left-to-right shunting | Maintain or decrease SVR | Avoid decreases in PVR | Avoid hyperoxia and hypocarbia (reduce FiO2 and minute ventilation). | Increases in SVR increase left-sided pressure, leading to an increase in left-to-right shunting. Similarly, a decrease in PVR also increases left-to-right shunting. General anesthesia with mechanical ventilation tends to decrease SVR but may also decrease PVR, so the net effect is difficult to predict. Generally, hyperventilation and hyperoxia should be avoided since these conditions lower PaCO2 and may lower PVR. Systemic hypotension may best be treated with phenylephrine because it will increase both SVR and PVR. |
| Fontan physiology (cavopulmonary palliation) | Decrease PVR Maintain preload Maintain contractility | Avoid increases in PVR Avoid hypovolemia Avoid myocardial depressants | Avoid or treat hypoxia, hypercarbia. Maintain appropriate analgesia with sedation or anesthesia. Maintain adequate preload with fluid replacement. Initiate inotropic support if necessary. | Pulmonary blood flow depends on both adequate RAP (as there is no pumping chamber) and low PVR. Treatment is aimed at both maintaining right-sided filling pressure (hypervolemia) and decreasing PVR (avoiding hypoxia or hypoventilation). Myocardial depression may reduce single ventricle performance and lead to an increase in the common atrial pressure, thus decreasing the transpulmonary pressure gradient, resulting in higher Fontan pressures. |
| Pulmonary hypertension | Decrease PVR Maintain preload | Avoid increases in PVR Avoid hypovolemia | Continue preoperative medications that minimize PVR. Avoid or treat hypoxia or hypercarbia. Consider inhalational pulmonary vasodilators (eg, nitric oxide or epoprostenol) for refractory increases in PVR. | Often, little can be done to reduce chronically elevated PVR; therefore, measures should be directed at avoiding further increases. Anesthetics lower PVR, particularly inhalational or volatile agents (exceptions are N2O and ketamine). This is especially true if administration of anesthetic agents is combined with mechanical ventilation with modest hyperventilation and increased FiO2 (both lower PVR). |
| Obstructive lesion | Maintain sinus rhythm and normal HR Maintain preload Maintain SVR | Avoid tachycardia/SVT Avoid severe bradycardia Avoid junctional rhythm Avoid hypovolemia Avoid vasodilation | Control HR. Perform cardioversion for hemodynamically unstable SVT. Maintain intravascular volume status with fluid replacement. Administer a vasoconstrictor. | Stroke volume across obstructive lesions is diminished due to elevated pressure gradients. A drop in SVR leads to hypotension as stroke volume is relatively fixed and cannot adequately increase to compensate. With atrioventricular (mitral or tricuspid) valve stenosis, a slower heart rate allows a longer diastolic period and promotes flow across the stenotic lesion. Maintaining sinus rhythm allows atrial contraction to contribute to ventricular filling. With aortic or pulmonic stenosis, a slower heart rate reduces myocardial work and allows time for ventricular filling and ejection across the stenotic valve. With valvular stenosis, both tachycardia and hypotension can contribute to myocardial ischemia by increasing oxygen demand and decreasing oxygen supply. |
| Regurgitant lesion | Normal to fast HR Decrease SVR | Avoid bradycardia Avoid hypertension | Treat bradycardia with glycopyrrolate, atropine, or ephedrine. Treat hypertension with vasodilators. Maintain appropriate analgesia with sedation or anesthesia. | With regurgitant lesions, the objectives are to maintain forward flow and to diminish backward or retrograde flow. With atrioventricular (mitral or tricuspid) regurgitation, the objective is to lower impedance to ejection of blood from the LV or RV. Thus, vasodilatation tends to favor forward flow. With aortic or pulmonic regurgitation, bradycardia prolongs diastole and promotes more regurgitation. Thus, maintaining a high normal HR is generally preferred. |
| Heart transplant | Maintain contractility Maintain SVR Maintain HR Lower PVR | Avoid myocardial depressants | Treat hypotension or bradycardia with direct-acting agents. Hypotension due to vasodilation is treated with phenylephrine or vasopressin (vasopressin is preferred over phenylephrine to minimize effects on PVR). Poor contractility is treated with epinephrine or norepinephrine. Bradycardia is treated with epinephrine or isoproterenol. | Transplant recipients often have early and/or late ventricular dysfunction due to causes including allograft ischemic injury, rejection, and cardiac allograft vasculopathy. Current cardiac function should be assessed and managed as needed. |
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