Heart Failure & Inotropes

Classifications of heart failure:

New York Heart Association Classification: based on symptoms.  Unlike ACC/AHA stages (see below), patients can shift classes based on medical therapy.

• Class I - symptoms with more than ordinary activity, no impairment of ordinary activities
• Class II - symptoms with ordinary exertion (e.g. walking 2 blocks, 1 flight of stairs)
• Class III - symptoms with minimal exertion - i.e. walking slowly around the house
• Class IV - symptoms at rest

ACC/AHA Stages of CHF: as opposed to NYHA, emphasizes progression of heart failure as a continuum; patients can NOT move back up in the stages

• Stage A - high risk for heart failure, but no structural heart disease (e.g. HTN, DM)
• Stage B - structural heart disease (e.g. valvular problem, prior MI) but never had any symptoms of CHF
• Stage C - prior or current symptoms of CHF --> majority of CHF patients
• Stage D - refractory/end stage CHF

 

 

DDx of cardiomyopathy:
#1 cause is Ischemic, followed by Hypertensive, Valvular, and Congenital (e.g. ASD).

 

Once the above are ruled out, you should investigate more unusual causes of cardiomyopathy.

-Infectious Myocarditis – Viral (Coxcackievirus, Echovirus, HIV), TB, Fungal, Toxoplasmosis, Chaga's Disease, others
-Toxic – Alcohol, Chemotherapy (i.e. anthracyclines), Cocaine/Amphetamines
-Autoimmune – Collagen Vascular Disease, Giant Cell Myocarditis, Peripartum
-Infiltrative – Hemochromatosis, Sarcoidosis, Amyloidosis
-Stress-induced (Takotsubo)
-Tachycardia-induced
-Familial/Genetic
-Metabolic – Hypo/Hyperthyroidism, Acromegaly, Pheochromocytoma, Beriberi, Selenium Deficiency
-Hypersensitivity/Eosinophilic Myocarditis

This is not an exhaustive list but a pretty good start.

 

 

 

Spectrum of CHF: Congestion and Perfusion. 
One framework for CHF involves taking into account congestion (wet vs dry) and perfusion (warm vs cold). 
· Assessing Congestion - Orthopnea, PND, JVD, Edema, Lung crackles, Hepatojugular Reflux
· Assessing Perfusion - Narrow pulse pressure, Tachycardia, Cool extremities, Decreased urine output, Altered mental status

               Dry      Wet
    Warm     A         B
    Cold       C         D
  
· Profile A is those with compensated, chronic CHF - goal for these pts is to uptitrate their cardiac meds (i.e. beta blockers, ACEI's) as tolerated.
· Profile B is probably the majority of CHF exacerbations we admit - volume overloaded, but still with adequate perfusion.  Goal for those patients is generally diuresis, with the goal of getting them back to profile A.
· Profile C is fairly uncommon, but highlights the fact that even pts with CHF can be hypovolemic.
· Profile D (Cold and Wet) is consistent with low output heart failure and cardiogenic shock - it is the most ominous one and carries the worst prognosis.  For these pts, they certainly need to be hospitalized, and generally their beta blockers should be held, and consideration given to IV inotropes (see below) and possibly IV vasodilators as well.

 

 

 

Symptoms:

• While shortness of breath is the most common symptom, can present with fatigue, abdominal pain, nausea/vomiting
• While left-sided failure is the most common cause of right-sided failure, fillings pressures have to be markedly elevated for them to occur – when present, one should think about infiltrative processes or constrictive physiology

 

Common precipitants of decompensation:

• Ischemia/infarction
• Arrhythmia
• Hypertension
• Valvular disease (in patients s/p TAVI, worry about both perivalvular and valvular regurgitation)
• Progression of systolic dysfunction
• RV pacing with induction of ventricular dyssynchrony
• Dietary nonadherence
• Medications (both nonadherence, and new meds such as negative inotropes and NSAIDs)
• Renal failure
• Pulmonary embolism

 

Remember that patients with diastolic dysfunction do not tolerate tachycardia/arrhythmias (loss of atrial kick), hypertension (increases LV wall stress), and ischemia (increases LV stiffness)

• With this physiology, they are predisposed to “flash” pulmonary edema: given the upward shift of the LV end-diastolic pressure-volume curve, for a given volume, filling pressures will be higher, which can lead to elevated left atrial pressures and pulmonary edema
• Once this occurs, it triggers a sympathetic response, which leads to hypertension, myocardial ischemia, and increased LV stiffening, which further shifts the pressure-volume curve upward, resulting in more pulmonary edema/hypoxia and worsening the cycle

 

Unlike in systolic heart failure, medical therapy for diastolic heart failure is not disease-modifying, and has not been shown to improve mortality

• The mainstays of therapy are BP control to stop/reverse LVH, optimization of volume, rate control if atrial fibrillation is present, and revascularization

 

 

Management of cardiogenic shock: Inotropes
· Main choices are Dobutamine, Dopamine, Milrinone, and Epinephrine
· Dobutamine is generally the drug of choice - beta 1 and 2 agonist = inotropy, but watch for arrhythmias, and possible hypotension (due to vasodilatory Beta-2 effect)
· Dopamine is beta and alpha agonist (at higher doses) so get vasoconstriction as well as inotropy, but super-arrhythmogenic, and increase in cardiac output is limited by increase in afterload
· Milrinone is a phosphodiesterase inhibitor: powerful inotrope, but also has a powerful vasodilatory effect - can cause severe hypotension.  Also, less titratable due to long half-life, and renal metabolism is a problem - so often not used acutely.
· Epinephrine acts on beta 1, 2, and alpha receptors - best for low cardiac output plus low SVR state (i.e. cardiogenic plus septic shock).
· Keep in mind that IV inotropes have not been shown to improve mortality in RCTs; in fact, retrospective data suggests that inotropes are associated with increased mortality --> keep in reserve for severe, decompensated CHF pts, not for routine use

 

 

(Christopher Woo MD, 1/18/11)

(Chanu Rhee MD, 6/11/10, 7/30/10 & 8/20/10)