advanced heart failure patients in er: tips and tricks cristina tita, md advanced heart failure and...
TRANSCRIPT
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!!