1. TREATMENT OF ACUTE DECOMPENSATED HEART FAILURE

2. OUR PATIENT 57y male from Bloemfontein
Presented to National District Hospital with:
Progressive dyspnoea
4 pillow orthopnoea
PND
Anasarca
Known to Cardiology department with:
Cardiomyopathy of unknown etiology
Medication:
Lasix 160mg bd
Dilatrend 25mg bd
Aldactone 25mg daily
Zocor 20mg daily
Aspirin 150mg bd
Enalapril 10mg bd

3. ACUTE DECOMPENSATED HEART FAILURE
The following recommendations are in agreement with:
The 2009 focused update of the 2005 American College of Cardiology/American Heart Association (ACC/AHA) heart failure guidelines
The 2006 Heart Failure Society of America (HFSA) guidelines for ADHF
The 2008 European Society of Cardiology (ESC) guidelines for acute heart failure

4. DRUG THERAPY
Oxygen Loop diuretics eg Furosemide Thiazide diuretics Enalapril Cozaar Carvedilol Atenolol Hydralazine Nitrates Spironolactone Digoxin

5. GOALS OF THERAPY Improve symptoms Optimize volume status
Identify etiology
Identify precipitating factors
Optimize chronic oral therapy
Minimize side effects
Identify patients who might benefit from revascularization
Educate patients concerning medications and self assessment of HF
Consider and, where possible, initiate disease management program

6. OXYGEN
The 2009 focused update of the 2005 ACC/AHA guidelines recommend :
Oxygen therapy to relieve symptoms related to hypoxemia
Routine administration of supplemental oxygen in the absence of hypoxia is NOT recommended
For patients requiring supplemental oxygen, consider initial therapies in the following order:
Non-rebreather face mask delivering high-flow percent oxygen.
If respiratory distress, respiratory acidosis, and/or hypoxia persist:
Non invasive positive pressure ventilation (NPPV) as the preferred initial modality
Patients with respiratory failure who fail NPPV, or do not tolerate or have contraindications to
NPPV:
Intubation for conventional mechanical ventilation
Once initial therapy has begun, oxygen supplementation can be titrated in order to keep the patient comfortable and arterial oxygen saturation above 90 %

7. DIURETICS
Patients with ADHF are usually volume overloaded. Volume overload, regardless of etiology, should be treated with intravenous diuretics as part of their initial therapy. Patients with aortic stenosis with volume overload should be diuresed with caution. Diuretic therapy without delay in the emergency department or outpatient clinic as early intervention may produce better outcomes IV rather than oral administration is recommended because of greater and more consistent drug bioavailability. DOSE: Furosemide — 40 mg intravenously Individualized and titrated according to response Patients who are treated with loop diuretics chronically are usually treated with a higher dose in the acute setting Peak diuresis typically occurs after 30 min MONITORING: Volume status and urine output s-K and s-Mg daily

8. DIURETICS
HEMODYNAMIC EFFECTS: By reducing intravascular volume, diuresis will eventually lower central venous and pulmonary capillary wedge pressures
Furosemide have an initial morphine-like effect in acute pulmonary edema, causing venodilation that can decrease pulmonary congestion prior to the onset of diuresis.
Diuretics may enhance the hypotensive effects of ACE-I or ARB therapy
RENAL EFFECTS: Renal function frequently deteriorates during diuretic treatment and careful monitoring is recommended
Worsening renal function during diuretic treatment of HF is an indicator of poor prognosis
Guidelines for management of patients with ADHF with abnormal or rising serum creatinine and/or urea include the following:
If serum creatinine rises modestly in the face of continued signs and symptoms of congestion, diuresis is generally continued.
If increases in serum creatinine appear to reflect intravascular volume depletion, then reduction or temporary discontinuation of diuretic or vasodilator therapy should be considered.
Patients with moderate to severe renal dysfunction and evidence of intravascular fluid overload should continue to be treated with diuretics. In the presence of severe fluid overload, renal function may improve with diuresis.
If substantial congestion persists and diuresis cannot be achieved without an unacceptable degree of renal impairment, then ultrafiltration or dialysis should be considered.
INADEQUATE RESPONSE :
Sodium and fluid restriction
Doubling the diuretic dose
Addition of a thiazide diuretic
Addition of spironolactone
A continuous intravenous infusion of the loop diuretic.
Ultrafiltration may be considered.

9. VASODILATORS
The HFSA guidelines provide the following recommendations for use of vasodilators:
In the absence of symptomatic hypotension, intravenous nitroglycerin may be considered as an addition to diuretic therapy for rapid improvement of
congestive symptoms in patients admitted with ADHF.
Frequent blood pressure monitoring is recommended with vasodilator agents. Dosage of these agents should be decreased if symptomatic hypotension develops
Intravenous nitroglycerin and diuretics are recommended for rapid symptom relief in patients with acute pulmonary edema or severe hypertension
Intravenous nitroglycerin may be considered in patients with ADHF and advanced HF who have persistent severe HF despite aggressive treatment with diuretics and standard oral therapies.
Nitrates are the most commonly used vasodilators. An initial dose of 5 to 10 µg/min of intravenous nitroglycerin is recommended
Nitroglycerin:
Reduces LV filling pressure primarily via venodilation.
At higher doses the drug variably lowers systemic afterload and increases stroke volume and cardiac output
Potential adverse effects of nitroglycerin include :
Hypotension
Headache
Nitrate administration is contraindicated after use of PDE-5 inhibitors such as sildenafil
Intravenous rather than oral nitrate administration :
Greater speed and
Reliability of delivery
Ease of titration
Similar benefits have been described with high-dose IV isosorbide dinitrate
If hypotension occurs, the longer half-life is a major disadvantage.

10. ACE-I & ARB
For patients with HF due to systolic dysfunction, ACE inhibitors and angiotensin receptor blockers (ARBs) are a mainstay of chronic therapy
Continued therapy 
For the majority of patients with systolic dysfunction who have been treated, maintenance oral therapy can be continued
Discontinue in the following settings:
Hypotension
Acute renal failure
Hyperkalemia
With regard to hypotension, two additional points should be considered:
Some patients tolerate relatively low blood pressures
Patients with acute pulmonary oedema may initially be hypertensive due to high catecholamine levels during the early period of distress
With initial therapy, blood pressure may fall rapidly and patients may become relatively hypotensive
Thus, long-acting drugs, such as ACE inhibitors and ARBs, should be administered with caution the first few hours of hospitalization.
Initiation of therapy 
Limited data on the safety and efficacy of initiating new ACE inhibitor or ARB therapy in the early phase of therapy of ADHF (ie, the first 12 to 24 hours)
Major concerns with early therapy include:
Hypotension and/or worsening renal function
Patients at high risk for hypotension (eg, low baseline BP or hyponatremia), which is a marker for increased activation of RAAS
Increased dependence upon angiotensin II for blood pressure maintenance
Aggressive diuretic therapy typically given for acute pulmonary oedema may increase sensitivity to ACE inhibition or angiotensin blockade
Once the patient is stable, chronic oral therapy with ACE inhibitor or ARB can be started

11. BETA-BLOCKERS
Beta blockers reduce mortality when used in the long-term management
Use cautiously in patients with decompensated HF with systolic dysfunction
Systolic dysfunction and ADHF, approach the use of beta blockers in the following manner:
Patients on chronic beta blocker therapy:
If the degree of decompensation is mild without hypotension or evidence of hypoperfusion, continuation of beta blocker as tolerated is recommended
 Moderate-to-severe decompensation or hypotension, decrease or withhold beta blocker therapy during the early phase of treatment
In patients requiring inotropic support or those with severe volume overload, withhold therapy
Patients not on chronic beta blocker therapy:
Do not initiate a beta blocker in the early management of acute HF
Initiate therapy prior to hospital discharge in stable patients
Start with low doses.

12. INOTROPES
As recommended in the 2009 ACC/AHA focused update, , intravenous inotropic or vasopressor drugs are recommended to maintain systemic perfusion and preserve end-organ function in:
Patients with evidence of hypotension associated with hypoperfusion AND obvious evidence of elevated cardiac filling pressures
Usefulness is uncertain for patients without elevated cardiac filling pressures
Similarly, the 2006 HFSA guidelines for ADHF include the following recommendations for use of inotropes:
Relieve symptoms and improve end-organ function in patients with advanced HF characterized by:
LV dilation
Reduced LVEF andlow output syndrome, particularly if these patients have marginal systolic blood pressure (<90 mmHg)
Symptomatic hypotension despite adequate filling pressure
Are unresponsive to, or intolerant of, intravenous vasodilators
Intravenous inotropes may be considered in patients with evidence of fluid overload if they respond poorly to intravenous diuretics or manifest diminished or worsening renal function.
Intravenous inotropes are not recommended unless left heart filling pressures are known to be elevated based on direct measurement or clear clinical signs.
Administration of intravenous inotropes in the setting of ADHF should be accompanied by continuous or frequent blood pressure monitoring and
continuous monitoring of cardiac rhythm.
Inotropes are not indicated for treatment of ADHF in the setting of preserved systolic function.
Routine use of inotropes in patients hospitalized for heart failure is not recommended

13. MORPHINE SULFATE 
Data are limited on the efficacy and safety of morphine therapy in ADHF
Morphine reduces patient anxiety and decreases the work of breathing
Diminish central sympathetic outflow,
Leading to arteriolar and venous dilatation
Resultant fall in cardiac filling pressures
Retrospective studies have found that morphine administration for ADHF is associated with:
Increased frequency of mechanical ventilation
Longer hospitalizations
More intensive care unit admissions
Greater mortality.
After risk adjustment and exclusion of ventilated patients, morphine remained an independent
predictor of mortality
Morphine therapy is not mentioned in the 2006 HFSA guidelines on management of ADHF or in the
2009 ACC/AHA focused update

14. OTHER
DIGOXIN
Given to patients to control symptoms or ventricular rate with AF
Possible effect on survival in chronic heart failure
NOT indicated as a primary therapy for the stabilization of patients with ADHF
ASPIRIN
No evidence for using aspirin in patients without coronary artery disease

15. SUMMARY Oxygen and assisted ventilation if needed
Diuresis with IV loop diuretic
Vasodilator therapy in patients without hypotension
SELECTED PATIENTS
IV positive inotropic agents
Mechanical cardiac assistance
Ultrafiltration