Transcript Advanced Heart Failure Patients in ER: tips and tricks

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/CMVseronegative 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 CMVseropositive 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
 Hook
 If
connections to controller and cables
up to power module if possible
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
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