Advanced Heart Failure Patients in ER: tips and tricks

CRISTINA TITA, MD

ADVANCED HEART FAILURE AND HEART TRANSPLANT PROGRAM

HENRY FORD HOSPITAL

Chronic Heart Failure Inability of the heart to maintain adequate organ perfusion or

ability to do so only at elevated filling pressures. Irrespective of LVEF

In a prospective evaluation of 413 patients hospitalized for HF, the relative risk for six-month mortality was lower for diastolic versus systolic HF dysfunction (13 versus 21 percent, adjusted HR 0.51).

Among 6076 patients discharged from a Mayo Clinic Hospitals in Olmsted County, Minnesota with a diagnosis of decompensated HF over a 15-year period (1987 to 2001), 53 percent had a reduced LVEF and 47 percent had a preserved LVEF. One-year mortality was relatively high in both groups, but slightly lower in patients with a preserved LVEF (29 versus 32 percent in patients with reduced LVEF, adjusted HR 0.96, 95% CI 0.92-1.00). Survival improved over time for those with reduced LVEF but not for those with preserved LVEF.

In a cohort of 2802 patients discharged from 103 hospitals in Ontario with a diagnosis of decompensated HF, one-year mortality was 22 percent in patients with a preserved LVEF versus 26 percent in patients with a reduced LVEF. This difference was not statistically significant.

Cardiac output/ peak oxygen consumption are better predictors of prognosis than LVEF.

“LVEF = heart’s age”

Decreased LVEF not a requirement for heart transplant listing

Decreased LVEF is a requirement for LVAD implantation, as LVAD assist with the ejection of blood from the heart, so the systolic function has to be significantly affected.

If patient on the heart transplant list will have a transplant pager

Presentation in Shock

Signs and symptoms of decreased end-organ perfusion

Hypoxia: how much oxygen is required?

Decreased systolic blood pressure: what is the diastolic blood pressure?

Lab abnormalities: increased lactate, abnormal LFT’s, renal markers, increased BNP +/- troponin, etc

Central line: SVC.

Venous oxygen saturation is highest in IVC > SVC > coronary sinus

Without direct measurement (Swan) MVS can be approximated by (3SVCS +IVCS)/4

SVC sat will be the closest to the mixed venous sat

Fick Cardiac output calculation: Oxygen consumption/ arteriovenous oxygen difference 135 ml/min/M2*BSA/ 13*Hgb*(SaO2-SvO2)

Sepsis/ Septic Shock

Low diastolic pressure, with MAP generally < 60

If you think of starting pressors in a heart failure patient, start antibiotics

Might not have fever, high WBCs

Venous saturation normal or high

Medium to high oxygen requirements; possible intubation

If needed use PEEP: even though PEEP decreases venous return and can decrease cardiac output; in septic heart failure patients the decrease in SVR will increase the CO/CI greatly over baseline

Adequate oxygenation very important especially given decrease oxygen utilization in context of sepsis

Ventricular arrhythmias (especially in ischemic cardiomyopathy patients) can be a presentation of sepsis (due to decrease oxygen uptake/ utilization)

Give fluids as needed: goal CVP ~ 15 (< 20).

Once sepsis resolves (patient coming off pressors, SVC sat decreasing) be very aggressive with fluid removal/ diuretics. The failing heart cannot cope with the massive fluid return once the vascular tone is back to normal.

Cardiogenic Shock

MAP generally preserved > 65-70 mmHg

Oxygen requirements generally low (exception: hypertensive urgency/ emergency)

SVC sat low (<60)

Decreased cardiac output

Elevated filling pressures

Start diuretics – low threshold for diuretic drips as natriuresis and diuresis better with drip even at equivalent dosing/ 24 hours

Remember Bumex: if patient with low albumin, Lasix/ torsemide will be less effective since they are dependent on albumin to reach the kidneys as well as to cross in the renal cells.

Always try vasodilators, with a goal MAP ~ 65 mmHg. Use IV NTG or nipride (short half life)

Do not start inotropes unless patient with severely decreased CO/CI AND not responding to afterload reduction

Arrhythmias

Do not use nondihydropyridine calcium channel blockers in patients with low EF, irrespective of how fast the atrial arrhythmia is.

If patient with atrial arrhythmia, unknown LVEF but fluid overloaded and ~ hypoperfused, assume LVEF decreased.

Atrial arrhythmias: IV digoxin, BB, amiodarone

Ventricular arrhythmias: IV BB, amiodarone. For unstable arrhythmias DCCV or defibrillation as appropriate.

Cardiac Transplantation: Rejection

Troponin will always be abnormal with severe acute rejection, either cellular or humoral due to myocite destruction

BNP might be elevated, depending on the acuity of presentation

Signs and symptoms of heart failure

Treatment in ER: IV salumedrol 1 gm

Cardiac Transplantation: Arrhythmias

Denervated heart: atropine will not be effective

Use isoproterenol if needed for symptomatic bradycardia, and pacing

Calcium channel blockers generally OK to use (if normal LVEF).

CCB preferred to BB due to graft survival benefit.

Supersensitivity of the sinus and atrioventricular (AV) nodes to acetylcholine and adenosine has been demonstrated after parasympathetic denervation

If using adenosine: half dosing (3 mg; max dose 6 mg)

Rule out rejection, especially for ventricular arrhythmias

For ventricular arrhythmias: amiodarone

Transplanted heart is dependent on the adrenergic input for adjustments in the cardiac output; if rejecting, stroke volume low, CO/CI will be dependent on the heart rate. BB can lead to cardiac arrest if given in acute rejection.

Cardiac Transplant: Infection

High suspicion, even with “general malaise” presentations

Might not have fever, high WBCs

Usual infectious work-up

Relatively low threshold for antibiotics

Remember CMV if anything is wrong

Check CMV PCR (not serology)

CMV is the most common and single most important viral infection in solid organ transplant recipients.

CMV infection usually develops during the first few months after transplantation and is associated with clinical infectious disease (eg, fever, pneumonia, GI ulcers, hepatitis.

Approximately 20% to 60% of all transplant recipients develop symptomatic CMV infection. The patients at highest risk for symptomatic disease are the CMV-seropositive donor/CMV-seronegative recipient (D+/R-) who develops a primary infection after transplantation. Such patients are at particular risk for severe manifestations of CMV infection, including tissue-invasive CMV and CMV recurrence.

Reactivation infection develops in the patient who becomes CMV-seropositive before transplantation, and is more frequent than primary CMV infection. 

LVADs

Left Ventricular Assist Device

A mechanical circulatory support pump that • unloads the ventricle

• provides continuous blood flow

• works in circuit with the patient’s heart

LVAD should be connected to power at all times

Batteries last ~ 12 hours; have indicators showing the charge

Thoratec HeartMate II Axial (continuous flow)

HeartWare HVAD & HeartMate III Centrifugal (continuous flow)

Inflow cannula (at LV apex)

Pump for continuous propulsion of blood

Outflow cannula (usually anastomosed to ascending aorta – though occasionally descending aorta or left subclavian artery)

Driveline

Controller

Batteries

LVAD alarms

**Alarm pamphlet good reference: can be found on www.thoratec.com

Red Heart Alarms require IMMEDIATE attention Have patient sit down, remain calm Check connections to controller and cables Hook up to power module if possible If still alarming quickly call VAD Emergency Pager

(313) 705-0089 and possibly call 911/code team

If cardiac arrest: listen to the chest: no compressions if LVAD hum present; only pharmacological

resuscitation and DCCV/ defibrillation as needed

If no LVAD hum: make sure power source is connected to the LVAD (document, patient would have red heart alarms as well): OK to do chest compressions.

LVAD without alarms

Diagnosis/ treatment as usual

Advantage: extra information provided by the LVAD monitors

Flow: cardiac output, but remember it is a calculated flow

Power: how much energy the machine uses to rotate at the set speed

PI (for HM II and HM III): contribution of the LV to the flow through the LVAD

LVAD flow normally ranges between 4-8 and is dependent on:

Left ventricular preload: depends on volume status and RV output

Afterload (systemic mean blood pressure)

LV contractility: LV contributes flow through LVAD and LVOT

Pump speed (set)

HeartMate II: ~8,000—12,000 RPM

HeartMate III: ~ 5000---6500 RPM

HeartWare: ~2,000—4,000 RPM

Check MAP: goal 65-80 mmHg; if out of range treat accordingly

If high flow: sepsis – will also have low PI

falsely high flow calculation due to high power use as seen in

Uncontrolled HTN

Pump thrombus: always check LDH in LVAD patients

If low flow: Hypovolemia

RV failure with low LV preload. Treat RV failure: diuretics, +/- inotropes, decrease in LVAD speed

LVAD power range: 4-8

Low power very uncommon: inflow cannula clot that would completely obstruct the flow through the LVAD

High power: High blood pressure

Clot in the the pump or the outflow tract (LDH)

PI = systemic resistance

PI relates to LV contribution to LVAD flow, will be increased when LV contribution higher; decreased when LV contribution lower

Normal range is 4-7

High PI

HTN

dehydration

Low PI:

Sepsis

Decreased resistance with bleeding AVM

Thank you for everything you do!!