Download Medical Treatment for acute Decompensated Heart Failure

Medical Treatment for acute
Decompensated Heart
Failure
Vlasis Ninios
Cardiologist
St. Luke’s Hospital
Thessaloniki 2011
2010 HFSA guidelines for ADHF
2009 focused update of the 2005
American College of Cardiology/American
Heart Association (ACC/AHA) HF
guidelines
2008 European Society of Cardiology
(ESC) guidelines for acute heart failure
General Approach
Clinical signs and symptoms
– Cough, dyspnea, fatigue
– Tachypnea, wheezing, hypertension,
hypotension, tachycardia
– Perfusion status
– Volume status
Precipitating Factors
MI, Ischemia
Arrhythmias (AF,VT, etc.)
Hypertension
Renal Failure
Anemia, infection, thyroid disease
Drugs
Tests
ECG
CXR
Lab data
BNP, pro-BNP
Echo
Cardiac catheterisation
Coronary angiography
Differential Diagnosis
Pulmonary embolism
Pneumonia
Asthma
ARDS
PATHOPHYSIOLOGY
Fluid transudation into the pulmonary
interstitium or alveolar spaces
Rapid and acute increase in left ventricular
filling pressures and left atrial pressure
Role of lymphatics
Predisposing conditions
Systolic dysfunction
Diastolic dysfunction
LVOT obstruction
Mitral stenosis
Treatment-general considerations
Hospital admission
– Hypotension, renal dysfunction,
hypoperfusion
– Rest dyspnea
– Arrhythmia
– ACS
MONITORING
Vital signs
Fluid balance, daily weight
Electrolytes, BNP, blood gas
Telemetry
Hemodynamic monitoring
Echo monitoring
Treatment goals
Hemodynamic stability, improve symptoms
Oxygenation, ventilation
Optimize volume status
Identify etiology
Identify and address precipitating factors
Optimize chronic oral therapy
Minimize side effects
Identify patients who might benefit from revascularization
Identify patients who might benefit from device therapy
Identify risk of thromboembolism and need for
anticoagulant therapy
Educate patients and relatives
Systolic vs diastolic
Similar: Diuresis, Oxygen, vasodilation
Hypertension and tachycardia
management in diastolic
Inotropes usually in systolic
Arrhythmia management
AF
– Rate control
– Cardiogenic shock (DC cardioversion)
VT
– DC shock
Initial stabilization
Airway assessment to assure adequate
oxygenation and ventilation, including
continuous pulse oximetry
Vital signs assessment with attention to
hypotension or hypertension
Continuous cardiac monitoring
Intravenous access
Seated posture
Diuretic therapy
Vasodilator therapy
Urine output monitoring
Oxygen and assisted vantilation
Face mask high flow of O2
noninvasive positive pressure ventilation
(NPPV)
Intubation- ventilation
Diuretics
No randomised trials but extensive experience
Hypotension, cardiogenic shock
Aortic stenosis
IV use is preferred
Loop diuretics
Dose similar to oral dose or 40-80 frusemide to
a naïve patient
Monitoring of urine, electrolytes, renal function
Beware of hypotension ie diastolic dysfunction
Diuretics and renal dysfunction
Other causes
If fliud overloaded, fluid removal
If Creatinine rises, consider inotropes
Ultrafiltration, dialysis
Diuretic resistance
Increase
Add thiazide (metolazone)
Continuous iv infusion
Ultrafiltration
Fluid restriction
Vasodilator therapy
Nitroglycerine, nitroprusside, nesiritide
Absence of hypotension and congestive
symptoms
Pulmonary edema and hypertension
Nitroglycerine
Venodilation, reduces LV filling pressure
Reduces afterload at higher doses
Tachyphylaxis
Never with sildenafil
Iv administration
Nitroprusside
Potent venous and arterial dilator
Reduces afterload
Hypertensive emergencies, acute AR,
acute MR
Beware of cyanide toxicity
Reflex tachycardia
Usually for 24-48 hrs
Nesiritide
Recombinant human BNP
Initial trials have shown favourable
hemodynamic effects and symptom relief
No effect on mortality (some concerns towards
increase in mortality)
Conflicting results on the effect on renal function
Alternative in patient without hypotension and
persistent symptoms despite conventional
therapy. Close monitoring is recommended
Additional therapy
ACE inhibitors and ARBs
B-blockers
Inotropes
DVT prophylaxis
Morphine
ACE-I and ARBs
Continued therapy
– Decrease or stop in Hypotension, Acute Heart
Failure, Hyperkalemia
Initiation of therapy
– Best NOT to initiate early (12-24 hours)
– Borderline blood pressure, hyponatremia
– Exception is in AMI
B-blockers
Reduce mortality long-term
Cautious use in acute phase of patients with
systolic dysfunction
If on chronic therapy, continue if tolerated
(OPTIMISE HF, Italian survey on AHF)
Decrease or withdraw if patient is compromised
Do not initiate in the acute phase
Initiate prior to discharge in stable patients (no
evidence of fluid retention)
Low dose and careful titration
Inotropes
Severe systolic LV dysfunction and low output
state
Hypotension
Elevated filling pressure
Evidence of end-organ hypoperfusion
Continuous monitoring is essential
Increase heart rate and myocardial O2 demand
May provoke arrhythmias
OPTIME-CHF (Milrinone vs palcebo).
Hypotension and arrhythmias
Milrinone
Phosphodiesterase inhibitor
Potent positive inotrope
Reduces systemic and pulmonary vascular
resistance
Improves LV diastolic compliance
Concomitant use of b-blockers does not diminish
drug effect
OPTIME-CHF (Milrinone vs palcebo).
Hypotension and arrhythmias. Worse outcome in
IHD
Dobutamine
B1 receptor agonist
Increase SV and CO
Modest decrease in SVR and PWP
“Dobutamine holiday”
No survival benefit
Effect is offset by b-blocker use (carvedilol
more than metoprolol)
Levosimendan
Enhance myocardial response to a given calcium
concentration
Reduction in cardiac filling pressures and increase in
cardiac index
Active metabolite that persists for up to 5 days
LIDO trial acute hemodynamic effects were superior to
Dobutamine, survival benefit at 6 months
RUSSLAN trial post MI, trend to survival benefit at 6
months
SURVIVE and REVIVE trials no benefit or harm in
mortality
DVT prophylaxis
LMWH, fondaparinux
Morphine sulphate
Limited data
Reduces anxiety and work of breathing
Arteriolar and venous dilatation due to
reduction of sympathetic outflow
Some safety concerns
Avoid unless in AMI
ULTRAFILTRATION
ADVANTAGES
– Effective, adjustable rates
– No effect on electrolytes
– Decreased neurohumoral activity
Renal failure, diuretic resistance,
excessive fluid overload
RAPID-CHF, UNLOAD, more effective
fluid removal, less hospitalizations
No safety data
Vasopressin receptor antagonists
Tolvaptan
– EVEREST trial, SALT-1 and 2, SALTWATER
– Increase Na by water excretion
– Limitations
Thirst
Neurological events by rapid Na correction
Cost
Conclusion
Accurate assessment, rapid diagnosis, lifesaving measures are essential
O2, diuretics, vasodilators mainstay of treatment
Close monitoring is essential
Ultrafiltration, and/or inotropes may be required
Mechanical assistance in severely compromised
patients
ACE-I and b-blockers are best initiated after
initial stabilization has been achieved