- Email: [email protected]
MY APPROACH to the patient with right ventricular failure
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E N D S I N
C
A R D I O V A S C U L A R
M
E D I C I N E
25 (2015) 471–472
Available online at www.sciencedirect.com
www.elsevier.com/locate/tcm
MY APPROACH
MY APPROACH to the patient with right ventricular failuren
Marc A Simon, MD, MS, FACC Right ventricular (RV) failure is a complex and difficult-totreat syndrome occurring in the setting of many diseases. In the acute setting, my approach involves three fundamental questions: 1. What is the patient’s volume status? 2. What is the patient’s RV contractility? 3. What is the patient’s underlying etiology for RV failure?
Volume status Appropriate management of volume status is crucial for the patient with RV failure. The volume-overloaded RV has reduced contractility and may also reduce LV filling and function via septal shifting (ventricular interaction). High venous pressure is associated with decreased renal function. Consider a stepwise approach to diuretics:
n
Start with intermittent IV furosemide (same or greater than the outpatient dose). Up-titrate furosemide to 80 mg three times daily; one can go higher, but, generally beyond this dose or in the critically ill patient, continuous IV drip should be considered. In the patient on bumetanide, use the same dose IV (although oral bioavailability is high, the volume-overloaded RV failure
patient is likely to have bowel wall edema preventing effective absorption). The equivalent IV dose of furosemide intermittently or a continuous IV drip can also be used. Adding a thiazide diuretic is another option, as is continuous IV bumetanide. A good rule of thumb is to keep in mind the patient’s medical records. Avoid repeating past diuretic failures, and use what has worked in the past as an effective guide. Renal function will improve with diuresis at a surprising frequency. However, in the patient with poor urine output and/or progressive renal failure consider adding an inotrope if low cardiac output is suspected (see below) and/or mechanical removal of fluid with hemodialysis/ultrafiltration (which may need to be continuous instead of intermittent if the patient is critically ill and/or systemic blood pressure is too low). Review sodium and fluid restrictions with patients.
RV contractile state Initial assessment of the patient should include a critical eye toward sufficient cardiac output. While a simple yes or no question, the signs and symptoms can be subtle. On history, warning signs of low output include poor appetite, weight loss (may be masked by fluid weight gain), and fatigue. In the physical exam, warning signs include cool extremities and cyanosis, poor urine output, and signs of hepatic congestion and failure (scleral icterus, overt jaundice, in particular; enlarged/pulsatile liver may just reflect volume overload). Most patients with RV failure will have somewhat low systemic blood pressure chronically but a pressure lower than their usual may indicate low cardiac output. If signs and symptoms suggest low cardiac output, then prompt institution of inotropes are indicated. I prefer to use milrinone because it is also a pulmonary vasodilator, which will decrease RV afterload. Be alert for vasodilation and ventricular arrhythmias. In the case of vasodilation, use or switch to dobutamine. Depending on your institution, inotropes may require the patient to be moved to the ICU.
First published on PracticeUpdate on October 06, 2014. Republished with permission.
http://dx.doi.org/10.1016/j.tcm.2014.10.029 1050-1738/& 2015 Published by Elsevier Inc.
472
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A R D I O V A S C U L A R
If there is significant hypotension, then start a vasopressor as needed. The key to this is to determine when blood pressure is too low; a good rule of thumb is systolic blood pressure 20% below the patient’s usual. I prefer dopamine, but vasopressin can be a good option, as can norepinephrine (which may also have some positive inotropic effect) or phenylephrine. These patients should be in an ICU.
ME
D I C I N E
25 (2015) 471–472
started without invasive hemodynamics documenting pulmonary arterial hypertension (mean pulmonary arterial pressure 425 mmHg, with a left-sided filling pressure r15 mmHg). Second, outside of the critically ill patient in the ICU, insurance approval for continuing the medications on discharge can require several weeks, and therapy should not be started until it can be confirmed that it will continue when the patient is discharged.
Etiology of RV failure When to check invasive hemodynamics There are many potential underlying causes of RV failure that lead to individualized evaluation and treatment. Think about systolic LV heart failure/cardiomyopathies (heart failure treatment as above; consider heart transplant evaluation depending on circumstances), coronary artery disease (RV infarction; consider coronary angiography and intervention), congenital heart disease (consider atrial septal defects in those with an enlarged RV but normal pulmonary pressures, which can present at any age), pulmonary hypertension (including pulmonary embolus), intrinsic lung disease, hepatic failure, and primary myopathies. With specific regard to the patient with RV failure from pulmonary hypertension, there are several unique therapeutic options. Inhaled nitric oxide can be used in the mechanically ventilated ICU patient, but the cost can be prohibitive; so, acute start of a prostacyclin should be considered. Epoprostenol (administered either IV or inhaled through a ventilator) can be rapidly up-titrated, but note that these patients have a very poor prognosis, which should be communicated with the patient and/or family. Caution should be advised in starting pulmonary vasodilators in two regards. First, pulmonary vasodilators should never be
If checking invasive hemodynamics, ask yourself two questions: how will this change or guide therapy, and will the line be removed immediately or kept in for a period of time (in the ICU) to further guide therapy? Invasive hemodynamics should be checked in the following circumstances: 1. Critically ill patients in whom knowledge of the filling pressures and cardiac output can influence your therapy 2. Clinical confusion between signs/symptoms and/or response to therapy 3. Assessment once euvolemia is reached (ie, pulmonary hypertension if considering starting or changing treatment or confirming true euvolemia and adequate cardiac output in the heart failure patient)
Assistant Professor of Medicine Heart Failure and Cardiac Transplantation University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania E-mail address: [email protected]
E N D S I N
C
A R D I O V A S C U L A R
M
E D I C I N E
25 (2015) 471–472
Available online at www.sciencedirect.com
www.elsevier.com/locate/tcm
MY APPROACH
MY APPROACH to the patient with right ventricular failuren
Marc A Simon, MD, MS, FACC Right ventricular (RV) failure is a complex and difficult-totreat syndrome occurring in the setting of many diseases. In the acute setting, my approach involves three fundamental questions: 1. What is the patient’s volume status? 2. What is the patient’s RV contractility? 3. What is the patient’s underlying etiology for RV failure?
Volume status Appropriate management of volume status is crucial for the patient with RV failure. The volume-overloaded RV has reduced contractility and may also reduce LV filling and function via septal shifting (ventricular interaction). High venous pressure is associated with decreased renal function. Consider a stepwise approach to diuretics:
n
Start with intermittent IV furosemide (same or greater than the outpatient dose). Up-titrate furosemide to 80 mg three times daily; one can go higher, but, generally beyond this dose or in the critically ill patient, continuous IV drip should be considered. In the patient on bumetanide, use the same dose IV (although oral bioavailability is high, the volume-overloaded RV failure
patient is likely to have bowel wall edema preventing effective absorption). The equivalent IV dose of furosemide intermittently or a continuous IV drip can also be used. Adding a thiazide diuretic is another option, as is continuous IV bumetanide. A good rule of thumb is to keep in mind the patient’s medical records. Avoid repeating past diuretic failures, and use what has worked in the past as an effective guide. Renal function will improve with diuresis at a surprising frequency. However, in the patient with poor urine output and/or progressive renal failure consider adding an inotrope if low cardiac output is suspected (see below) and/or mechanical removal of fluid with hemodialysis/ultrafiltration (which may need to be continuous instead of intermittent if the patient is critically ill and/or systemic blood pressure is too low). Review sodium and fluid restrictions with patients.
RV contractile state Initial assessment of the patient should include a critical eye toward sufficient cardiac output. While a simple yes or no question, the signs and symptoms can be subtle. On history, warning signs of low output include poor appetite, weight loss (may be masked by fluid weight gain), and fatigue. In the physical exam, warning signs include cool extremities and cyanosis, poor urine output, and signs of hepatic congestion and failure (scleral icterus, overt jaundice, in particular; enlarged/pulsatile liver may just reflect volume overload). Most patients with RV failure will have somewhat low systemic blood pressure chronically but a pressure lower than their usual may indicate low cardiac output. If signs and symptoms suggest low cardiac output, then prompt institution of inotropes are indicated. I prefer to use milrinone because it is also a pulmonary vasodilator, which will decrease RV afterload. Be alert for vasodilation and ventricular arrhythmias. In the case of vasodilation, use or switch to dobutamine. Depending on your institution, inotropes may require the patient to be moved to the ICU.
First published on PracticeUpdate on October 06, 2014. Republished with permission.
http://dx.doi.org/10.1016/j.tcm.2014.10.029 1050-1738/& 2015 Published by Elsevier Inc.
472
T
R E N D S I N
C
A R D I O V A S C U L A R
If there is significant hypotension, then start a vasopressor as needed. The key to this is to determine when blood pressure is too low; a good rule of thumb is systolic blood pressure 20% below the patient’s usual. I prefer dopamine, but vasopressin can be a good option, as can norepinephrine (which may also have some positive inotropic effect) or phenylephrine. These patients should be in an ICU.
ME
D I C I N E
25 (2015) 471–472
started without invasive hemodynamics documenting pulmonary arterial hypertension (mean pulmonary arterial pressure 425 mmHg, with a left-sided filling pressure r15 mmHg). Second, outside of the critically ill patient in the ICU, insurance approval for continuing the medications on discharge can require several weeks, and therapy should not be started until it can be confirmed that it will continue when the patient is discharged.
Etiology of RV failure When to check invasive hemodynamics There are many potential underlying causes of RV failure that lead to individualized evaluation and treatment. Think about systolic LV heart failure/cardiomyopathies (heart failure treatment as above; consider heart transplant evaluation depending on circumstances), coronary artery disease (RV infarction; consider coronary angiography and intervention), congenital heart disease (consider atrial septal defects in those with an enlarged RV but normal pulmonary pressures, which can present at any age), pulmonary hypertension (including pulmonary embolus), intrinsic lung disease, hepatic failure, and primary myopathies. With specific regard to the patient with RV failure from pulmonary hypertension, there are several unique therapeutic options. Inhaled nitric oxide can be used in the mechanically ventilated ICU patient, but the cost can be prohibitive; so, acute start of a prostacyclin should be considered. Epoprostenol (administered either IV or inhaled through a ventilator) can be rapidly up-titrated, but note that these patients have a very poor prognosis, which should be communicated with the patient and/or family. Caution should be advised in starting pulmonary vasodilators in two regards. First, pulmonary vasodilators should never be
If checking invasive hemodynamics, ask yourself two questions: how will this change or guide therapy, and will the line be removed immediately or kept in for a period of time (in the ICU) to further guide therapy? Invasive hemodynamics should be checked in the following circumstances: 1. Critically ill patients in whom knowledge of the filling pressures and cardiac output can influence your therapy 2. Clinical confusion between signs/symptoms and/or response to therapy 3. Assessment once euvolemia is reached (ie, pulmonary hypertension if considering starting or changing treatment or confirming true euvolemia and adequate cardiac output in the heart failure patient)
Assistant Professor of Medicine Heart Failure and Cardiac Transplantation University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania E-mail address: [email protected]