POTD: All About LVADs

Hey everyone,

Today’s POTD will be all about LVADs, something we encounter rarely, but vitally important to know about. Feel free to skip to the bottom for the TL;DR!

What are LVADs?

Left ventricular assistance devices (LVADs) were developed in 1960s as a bridge to cardiac transplant, but is now also used as destination therapy, meaning it is the patient’s final therapy for heart failure during their lifetime. They are typically powered by two batteries with a power base unit that can be plugged into the wall. Indicated for NYHA class 4 HF, ejection < 25%. Note the Heartmate II is the most common one in use today.

Components

Pump: takes blood from cannula in apex of LV and pumps it directly into aorta.

Driveline: percutaneous cable that exits the abdominal wall and connects pump to external components such as controller and battery.

Controller: external “box” containing computer for device. Monitors pump performance and has controls for settings/alarms/diagnostics. Will show pump speed and output. Listed here are the normal range of values.

  • Pump Speed: 2200 – 2800 rpm (HeartWare VAD) and 8000 – 10000 rpm (HeartMate II VAD)

  • Power: 4 – 6 Watts

  • Flow: 4 – 6 L/min

  • Pulsatility Index (PI): 1 – 10

Power supply: connected to batteries or power base station which plugs into wall

FOR EMS PROVIDERS: In an emergency, all efforts should be made to transport patients with LVADs to their respective LVAD center. If a patient is brought to a non-device center, it is crucial that EMS personnel make every effort to bring the patient’s peripheral equipment needed to support them until they can be transferred to an LVAD center.

 

Common complications

Bleeding: most common reason for ED visit, most commonly in first month after implant. Tx with anticoagulant reversal, transfuse if needed. LVADs can cause acquired von Willebrand Disease, thought to be from the action of rotary or axial flow pump of the LVAD which causes high shear stress that may increase lysis of large vWF multimers.

Infection: from driveline and pocket, cover broadly with vanc/cefepime

Pump thrombosis: tx with heparin/antiplatelets or tPA in life-threatening situations. Pts will be on anticoagulation but pump thrombosis can still be common due to prosthetic material inflammatory reaction with blood and intrinsic endothelial activation in response to a continuous flow.

Arrhythmia: tx like you would in pt without LVAD either chemically or with electricity - place pads in anterior/posterior positioning

Suction event: when LV myocardium partially occludes the LVAD inflow cannula reducing inflow. Caused by low LV preload relative to pump speed. Tx by giving fluids, consider reducing LV speed in conjunction with LVAD team.

Cardiac tamponade: refer to LVAD center, pericardiocentesis discouraged b/c of low yield and potential for harm as the LVAD outflow graft may traverse typical course of needle.

Initial assessment FOCUSES ON CIRCULATION:

CONTACT THE LVAD TEAM: here at Maimo, the number is 35CHF

Note patients with LVADs will have NO PALPABLE PULSE and NO DISCERNIBLE HEART SOUNDS. Instead you will hear a continuous hum to confirm device is operating, though newest Heartmate 3 may have some interruptions to hum.

Measure the BP (must use doppler US and sphygmomanometer with doppler placed over brachial or radial artery).

1.        Cuff inflated until pulse no longer audible and then deflated.

2.        BP reading made when arterial flow audible again, giving single reading as MAP.

Goal MAP 70-80 and no more than 90 as this high afterload may compromise optimal function of LVAD. Should place A-line in hemodynamically unstable/hypotensive patients to more closely monitor BP.

Work-up will be the usual things you do for a cardiac patient: EKG, labs including trop, BNP, CXR. BEDSIDE ECHO AND COAGS/HEMOLYSIS LABS will be key because they can lead you down different diagnostic pathways.

Approach to conscious hypotensive patient with LVAD: check flow and power

Low flow vs high flow?

·      Low flow suggests hypovolemia

·      High flow state

o   Normal power or high power?

·      Normal power – distributive shock

·      High power – obstructive shock from thrombosis vs suction event vs cardiac tamponade

Differing schools of thought on CPR in LVAD:

Some argue you should analyze the LVAD first, others say you should begin CPR immediately if a patient comes in with circulatory collapse like you would any other patient.

If you were to analyze the LVAD first, then LOOK, LISTEN, FEEL:

Look at all connections

Listen for hum

Feel (hot control box usually means thrombosis or other obstruction)

Sometimes there is a hand pump attached to LVAD, but if pt unresponsive with MAP < 50 and etCO2 <20, or LVAD cannot be restarted, it is reasonable to proceed with CPR if you're in a setting without an LVAD team.

TL;DR of what to do when an LVAD patient arrives:

CONTACT THE LVAD TEAM through extension 35CHF here at Maimo.

  1. Patients with LVADs may have no palpable pulse and that is normal! You should hear a continuous hum on auscultation to verify that it is working.

  2. Look at all connections, listen for hum, analyze settings on the box.

  3. Measure the BP with a cuff and doppler and aim for a MAP of 70-80, no more than 90. An A-line should be placed for close hemodynamic monitoring.

  4. Do a bedside echo and get the usual labs but include hemolysis labs/coags.

  5. In a hypotensive patient with an LVAD, low flow is from hypovolemic shock; high flow will either be distributive (normal power reading) or obstructive shock (high power reading).

  6. Shocks are okay for the appropriate arrhythmias.

  7. If a patient is in circulatory collapse and the LVAD is not working/can't be restarted/there is no handpump, it is reasonable to proceed with CPR if you're in a setting without an LVAD team, but follow your institutional recs. Note that here at Maimo, it is advised not to start compressions.

References

https://emcrit.org/emcrit/left-ventricular-assist-devices-lvads-2/

https://criticalcarenow.com/when-a-vad-goes-bad/

https://www.uptodate.com/contents/emergency-care-of-adults-with-mechanical-circulatory-support-devices

https://first10em.com/lvads/

https://rebelem.com/left-ventricular-assist-device/

https://www.emdocs.net/lvad-patients-what-you-need-to-know/

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POTD: Trauma Tuesday - Vasopressors in hemorrhagic shock

Background pathophysiology:

Hemorrhagic shock is initially driven by a sympatho-excitatory phase attempting to compensate for acute blood loss and is characterized by vasoconstriction, tachycardia, and preserved MAP. The hypotension that subsequently follows is a result of decreased sympathetic nervous system activity from a physiologic exhaustion of endogenous catecholamines (norepi, epi) and other adjuncts (angiotensin II and vasopressin).

 

The traditional teaching:

The objectives of hemodynamic resuscitation in trauma is to restore adequate intravascular volume with a balanced ratio of blood products, correct pathologic coagulopathy, and maintain organ perfusion. The use of vasopressors has been traditionally discouraged in this setting as several studies have demonstrated that it leads to adverse outcomes and increased mortality risk. Permissive hypotension is advocated based on limited data that lower SBP and MAPs will result in improved mortality. Note that ATLS does not recommend the use of vasopressors currently.

 

Vasopressin as the pressor of choice for trauma?

The truth is that the optimal arterial blood pressure target for resuscitation of hemorrhagic shock patients is unknown. There are no studies that have come up with a concrete goal. In order to avoid increased mortality, we have shied away from using vasopressors as adjuncts in trauma resuscitation, but we know that intuitively, persistent hypotension and hypoperfusion are associated with worse coagulopathy and organ function. Thus, it would seem prudent to reconsider this all-or-nothing strategy for something more nuanced. In one of the landmark papers that demonstrated poor outcomes from early vasopressors by Sperry et al, vasopressin was the only vasopressor that was not associated with increased mortality.

 

In 2019, the AVERT-Shock trial demonstrated that vasopressin administration may improve blood pressure and perfusion without worsening blood loss or increasing mortality. Vasopressin has a direct vasoconstricting effect on V1 receptors but also increases the sensitivity of the vasculature to circulating catecholamines. This is why it is often used as a second-line agent in critical care settings. Theoretically, vasopressin may augment the effects of the limited endogenous catecholamines circulating when a body is in hemorrhagic shock and avoid the deleterious effects of adding exogenous ones.

 

However, note that this study included a much larger proportion of penetrating trauma compared to blunt trauma, potentially limiting generalizability. While it demonstrated a robust clinical difference, it was underpowered to show a statistically significant difference in mortality. Ultimately further investigations are needed, but this paper provides a great jumping off point into how we may reach for a more balanced approach to trauma resuscitation that may include both blood products AND vasopressors when the blood products alone do not seem to be restoring perfusion.

References

https://rebelem.com/avert-shock-vasopressin-for-acute-hemorrhage/

https://emcrit.org/wp-content/uploads/2022/04/Vasopressors_in_Trauma__A_Never_Event_.13.pdf

A. Sims et al., “Effect of Low-Dose Supplementation of Arginine Vasopressin on Need for Blood Product Transfusions in Patients With Trauma and Hemorrhagic Shock: A Randomized Clinical Trial,” JAMA Surg, Aug. 2019.

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POTD: Neonatal Resuscitation

We’ll be going over a few high yield topics pertaining to NALS today. 

It’s 7:30 AM, and you’ve just unwrapped your BEC sandwich and taken your first sip of coffee. You’re settling into the morning getting ready for your 12 hour peds shift… until the phone rings, and you get a note: 

“Mother 38w delivered her baby at home 30 minutes ago. Baby is having labored breathing, and is bradycardic. EMS will be here in 2 minutes.”

Take a deep breath. First, remember the basics. If you’re in a facility that has Peds/NICU, call them immediately. Call respiratory. Call pharmacy. Call Hector. Use the resources available to you. 

The set up.

Get the warmer and set it to 25 C

  • Avoid hypothermia in these patients. The goal is > 36.5-37.5C

Grab the Broselow tape so that it’s available for immediate use.
Get the backboard.
Grab the code cart, zoll
Get a towel to warm and dry the baby.
Get your airway equipment ready:

  • Suction x 2, plugged in, ready to go

  • Oxygen: grab the neonatal BVM and plug it into the oxygen port

  • Airway equipment: have both DL/VL equipment,

    • LMA size 1

    • Pre-loaded tubes

      • 2.5 and 3.0 uncuffed tubes

    • Blades: 0 and 1

    • EtCO2

Access: IO gun + pink needles ready for use; umbilical vein catheters (future POTD)

Grab your PALS card or open up your PediStat app
Ultrasound

Assess the patient.

Pediatric assessment triangle:

  • Appearance – crying? Good tone? Tracking?

  • Breathing – nasal flaring? Stridor? Grunting? Head bobbing?

  • Circulation – Pallor? Cyanosis? Mottling?

Off the bat, there are two numbers you need to remember:
HR < 100→ initiate positive pressure ventilation (PPV)
HR < 60→ initiate CPR / epinephrine if this is sustained more than 30 seconds despite adequate ventilation.

  • NOTE: Bradycardia is almost always related to hypoxia, so atropine isn’t routinely indicated for these patients.

Remember, the most important part of neonatal resuscitation is positive pressure ventilation.


PPV.

If the patient is spontaneously breathing but labored, you can place them on CPAP.
Remember, the targeted SpO2 after birth is much lower for neonates, so see the box below. You’re more interested in ventilating than the oxygenation.
For gasping / apneic / HR < 100 patients, initiate PPV. You can use 5 on the PEEP valve.

  • Rate: 40-60 breaths / minute

MR SOPA mnemonic for ventilation tips:

  • Mask, right size

  • Reposition airway

  • Suctioning nares

  • Open mouth

  • Pressure increase to PEEP to ~5

  • Advanced airway: ETT / LMA

BGM.

They also have lower BGMs. Hypoglycemia for neonates is < 30 for a patient < 24 hours old. It’s recommended to give D10 bolus 2ml/kg if the patient is hypoglycemic.

You can give glucagon IM too: 0.03mg/kg max 1mg

CPR.

It’s recommended to secure an airway (supraglottic or ETT) prior to doing compressions) since most these codes are usually due to respiratory events.
The ideal ratio is3 compressions:1 breath

  • Goal is 90 compressions: 30 breaths in one minute

2 thumb compression technique (*preferred) or 2 finger technique
Pulse checks q1 min
Depth: ⅓ chest diameter

Epinephrine.

IV dosing: 0.01mg/kg q3-5min
ETT dosing: You can give epinephrine through the ETT too if you don’t have access yet! AHA recommends a larger dose 0.1mg/kg of 1:1000 ETT

  • Max dose is 10mg, and follow it with a saline flush

I highly recommend reviewing the following flowchart linked.

I hope this was a good refresher on some of the most important concepts. I would love to learn other tips that others have in managing these stressful situations!

References:

https://cpr.heart.org/en/resuscitation-science/cpr-and-ecc-guidelines/neonatal-resuscitation 

https://emergencymedicinecases.com/neonatal-resuscitation/