Acute Decompensated HF Flashcards
Acute HF Syndromes
- Acute Myocardial infarction
- Acute valvular disease
- Fulminated myocarditis
- Acute on chronic diastolic heart failure
- Acute on chronic systolic heart failure
Acute on chronic systolic heart failure or ADHF Key Precipitants
• Non-compliance • Poorly controlled HTN • Ischemia/ACS • Afib or other arrhythmias • Infections • Pulmonary emboli • Worsening renal function -can be from HF meds or OTC
Hemodynamic Descriptors of ADHF
• Elevated cardiac filling pressures
(congestion)
• Reduction in cardiac output
Thus: Cold and Wet
Physical Exam Findings
- Elevated cardiac filling pressures:
-Rales
-JVP, hepatojugular reflux
-Hepatomegaly
-Ascites
-Edema - Low cardiac output:
- Narrow pulse pressure (PP
Goals of Therapy in ADHF
Fundamental GOAL: restore and maintain optimal filling pressures on diuretics and vasodilators!
• Relieve symptoms -deal w/elevated filling pressures! -thus diuretics and vasodilators • Optimize volume status • Identify etiology • Identify precipitating factors • Optimize chronic oral therapy • Minimize side effects • Educate patient/family
Current Tx for ADHF
- Diuretics-reduce volume
- Vasodilators-decrease preload and/or afterload
- Inotropes
- augment contractility
Diuretics in HF
- IV loop diuretics are mainstay of therapy for acute heart failure (given to ~ 90% of pts)
- Relieve symptoms of dyspnea and edema in most patients
• Associated with variety of potential problems:
-Electrolyte abnormalities
• wasting of K+, Na+, etc. can set you up for arrhythmias
- Activation of RAAS and SNS
- Diuretic resistance
- Worsening renal function
- Increased mortality?
*Loops won’t make it to the loop in pts w/renal issues because low RBF. Need higher dose
Diuretic Strategies in Patients with ADHF
Pts have decreased maximal response to diuretics and take higher doses to achieve same effect as normal
*higher doses are more effective but may cause worsening renal function
Tx of Warm and Wet Pt:
- Enhanced diuresis
- IV Loop diuretics (furosemide, bumetanide) - Not needed in most, but Some patients maybe IV vasodialtor leading to acute reductions in cardiac filling pressure
- venous: decrease preload
- arterial: afterload reduction - Usually don’t need to stimulate contractility to get diuresis
Tx of Cold and Wet
- Warm up before drying out
- IV vasodilator to decrease SVR to increase CO so that diuretics can actually get to loop (increase RBF) - IV Loop diuretics
- IV vasodilators
- main pro: reduction in mitral regurgitant flow
- MR can take up to 75% of EF! - Some may need to stimulate cardiac contractility (dobutamine, milrinone, DA)
Cold and Dry
- Assess for filling pressures that would actually make the patient cold and wet
- If PCWP less than 12 or RAP less than 5mmHg
- cautious fluid replacement orally - Limited Options
- Positive Inotropes may help temporarily
- BB may eventually help, but most can’t tolerate BB b/c limited contractile reserve
- Vasodilators may increase CO but probably just cause hypotension
IV Vasodilators:
Physiologic Rationale:
• Reduce preload (venodilation) and afterload (arterial dilation)
- Decrease mitral regurgitation (systemic vasodilation)
- Improve systemic cardiac output, tissue perfusion
- Decrease left atrial pressure, secondary pulmonary HTN
- Reduces RV afterload, decreases tricuspid regurgitation
- Decreases RA pressure
- IV administration allows for titration
Nitroglycerin
- Primarily a venodilator at lower doses (preload reduction)
- Rapid decline of pulmonary venous and LV filling pressures
- Reduction in dyspnea
- Decrease in myocardial O2 consumption
- Arterial dilator at higher doses
- Tolerance, headaches
Nitroprusside
- Powerful arterial and venous dilator
- Acts through its active metabolite nitric oxide
- Very short half-life (~2 min), rapid onset and offset of action
• Arterial vasodilation primarily at level of resistance vessels
• Coronary steal, hypoxemia
–kind of a paradox, but what happens is that vasodilation happens and blood goes to those that were dilated and not to the somewhat dz’d arteries
• Cyanide toxicity, particularly if renal function impaired
Nesiritide
• Recombinant form of brain natriuretic peptide
• Balanced vasodilator
• Increases cardiac output independent of changes in contractility
– because it reduces afterload
• Weak natriuretic, diuretic
• Longer half-life, risk of prolonged hypotension
