Wednesday, January 31, 2018

LVAD for the Nephrologist-Part 1

Advanced heart failure is associated with very poor survival rates of about 10 % at one year. Treatment options include cardiac transplantation or cardiac assist devices. A left ventricular assist device (LVAD) is a mechanical circulatory support for patients with advanced heart failure. Previously considered only as a bridge to transplant, these are becoming more common as a ‘destination’, and used in patients with end stage heart disease patients who are not heart transplant candidates. Of interest to us, this poor cardiac function in heart failure is often complicated by renal dysfunction, the so-called ‘cardio-renal syndrome’. This blog focuses on the outcomes of renal dysfunction in patients with LVAD and few aspects of renal replacement therapy (RRT) in them. I would discuss this in 2 parts to facilitate coverage of all aspects.
I will start with few basics of LVAD that helps in understanding the intricacies of monitoring in HD patients. LVAD consists of an inflow cannula that connects to the left ventricular apex and outflow cannula that connects to the aorta, ascending or descending. A pump connects these two cannulas. An external device, a system controller displays all the LVAD parameters and helps in adjusting the device settings. The pump connects to the controller via a drive-line/percutaneous lead that tunnels subcutaneously and exits the abdominal wall. The power supply is through two batteries that are worn by the patient all the time with adequate backups at their disposal, just in case (see image).
The anatomy and physiology of LVAD has changed over decades (see image below), from a pulsatile flow(pf)-LVAD which were big and relied on pneumatic compression system to pull in and out blood through vascular system to continuous flow(Cf)-LVAD which are more compact and use a power operated rotatory element for moving the blood. The complex structure, large size and the decreased durability were mainly responsible for pushing the pf-LVAD from the main stream and making them obsolete. They were frequently placed in the peritoneal cavity and patients were quite troubled from the noise produced by this device.
A Cf-LVAD is much smaller and does not have the complex structure associated with its predecessor. They are more durable and are usually placed in the abdominal wall (e.g. Heartmate 2) or in the pericardial space (e.g. Heartmate 3 or HVAD/Heartware). Two subtypes of Cf-LVAD exist depending on the type of rotatory pump. The axial flow pump rotates like a propeller in a pipe where in blood flows parallel to the pump and the centrifugal flow pump is a spinning disk with blades with outflow of blood tangential to the disk. Heartmate 2 and Heartmate 3/HVAD are examples of axial flow & centrifugal flow devices respectively.
A few points about LVAD parameters at this stage:
1) Pump speed- the only parameter in the LVAD that can be adjusted and directly influences the pump flow. Very high pump speeds may have consequences such a) hemolysis and platelet activation (due to shear stress on cells), b) supravalvular thrombosis (Cf-LVAD increase diastolic blood pressure -> decreases trans-aortic valve pressure gradient -> decreases frequency and duration of AV valve opening -> decreases blood flow through AV valve -> stasis of blood in the supravalvular region -> thrombosis), c) Right ventricular (RV) dysfunction (increased LVAD flow -> more unloading of left heart -> left shift of interventricular septum (IVS) -> increased RV cavity size -> impaired mechanics of RV contraction + pull over septal leaflet of tricuspid valve with regurgitation -> RV failure) and in extreme cases can lead to d) suction event (very high flow rates -> increased unloading of LV -> collapse of LV on the inflow cannula), which can be fatal as it decreases the outflow and causes arrthymia (IVS impinges on the cannula).
2) Pump flow – defines the amount of blood flowing through the LVAD pump in a minute. It can be as high as 10 L/minute. It is directly proportional to the pump speed and inversely to the head pressure (defined as pressure difference between the LV cavity and the aorta). A decrease in preload due to vasodilatation (drugs/sepsis) can increase the flow rate. On the contrary, hypovolemia (e.g. more ultrafiltration in dialysis), RV dysfunction, and tamponade decrease preload and subsequently the flow. Hypertension by increasing the afterload has a similar effect.
3) Pulsatility Index (PI) –a dimensionless variable which reflects the contractility of LV and it varies directly according to underlying LV function with low PI indicating worsening of LV function due to either a decrease in preload (again can happen in dialysis) or progression of underlying heart disease or an effect of negative inotropes on the right heart. During dialysis, it`s safe to maintain the PI.
How to monitor pulse and blood pressure in patients on LVAD? Well it`s tricky, as Cf-LVAD has a continuous flow physiology. So the pulse is not felt in more than half of these patients. Definitely scary to see a living person with no palpable pulse! The presence or absence of pulse depends on underlying LV function. And it`s even more difficult to monitor blood pressure. If patient has a radial pulse, we can measure pressure manually or with an automated machine. If pressures cannot be obtained with this, a Terumo device could be used for recording. This device has 2 cuffs- large & small which are more sensitive for low pulse pressure and hypovolemia. If radial pulse is not felt, then the best way to measure blood pressure is with the help of a Doppler. The cuff is tied over the upper arm and brachial artery is localized with Doppler. The cuff is inflated until the Doppler signal is lost. On slow deflation, the pressure at which the first Doppler signal is heard corresponds to the mean arterial pressure (MAP). So in patients with LVAD, we have essentially only one pressure recording, MAP of `x` mm Hg. It`s always advisable to maintain MAP between 70-80 mmHg. High MAP (especially greater than 90 mmHg) is associated with decrease in blood flow through the pump and thrombosis.

ACE inhibitors or ARBs are the drug of choice for hypertension control in these patients. Vasodilators are frequently used if MAP is very high. Negative inotropes especially non dihydropyridine calcium channel blockers need to be used with caution as they can impair RV function.

LVAD use is ever increasing in cardiology due to the increasing burden of heart failure patients. Its use has changed from being a bridge to transplantation to now being a destination therapy. As a greater number of patients with heart failure have renal dysfunction, LVAD use has implications for the nephrologist as well.

Post by Sriram Sriperumbuduri, Nephrology Fellow Ottawa

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