Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It has multiple causes and symptoms including shortness of breath, fatigue, fluid retention, and arrhythmias. Treatment focuses on controlling symptoms with diuretics, and improving the heart's function with ACE inhibitors, beta blockers, and other vasodilators. For severe cases, inotropic drugs or even advanced therapies like ventricular assist devices or transplant may be needed. The goals are to improve quality of life and survival through controlling risk factors and compensatory mechanisms that can worsen the condition over time.

1. Congestive Heart Failure
Heart failure is defined as the pathophysiologic state in which
impaired cardiac function is unable to maintain an adequate
circulation for the metabolic needs of the tissues of the body.

3. Causes

4. Symptoms
• Congested lungs
• Dizziness, fatigue, and weakness.
• Fluid and water retention
• Severe shortness of breath.
• Arrythmias.
• Coughing up foamy, pink mucus.

5. Classification
• Systolic versus diastolic
– Systolic- loss of contractility
– Diastolic- decreased filling or preload
• Left-sided versus right –sided
– Left- lungs
– Right-peripheral
• Acute versus chronic
– Acute- MI
– Chronic-cardiomyopathy

6. Classification of Heart Failure
• AHA (American Heart Association) Guidelines
– Stage A – High risk of HF, without structural heart
disease or symptoms
– Stage B – Heart disease with asymptomatic left
ventricular dysfunction
– Stage C – Prior or current symptoms of HF
– Stage D – Advanced heart disease and severely
symptomatic or refractory HF

8. Pathophysiology of CHF
• Pump fails → decreased stroke volume /CO.
• Compensatory mechanisms kick in to increase CO
– SNS stimulation → release of epinephrine/nor-
epinephrine
• Increase HR
• Increase contractility
• Peripheral vasoconstriction (increases afterload)
– Myocardial hypertrophy: walls of heart thicken to provide
more muscle mass → stronger contractions

9. Pathophysiology of CHF
– Hormonal response: ↓’d renal perfusion
interpreted by juxtaglomerular apparatus as
hypovolemia. Thus:
• Kidneys release renin, which stimulates
conversion of antiotensin I → angiotensin II,
which causes:
– Aldosterone release → Na retention and water
retention (via ADH secretion)
– Peripheral vasoconstriction

10. Pathophysiology of CHF
• Compensatory mechanisms may restore CO
to near-normal.
• But, if excessive the compensatory
mechanisms can worsen heart failure because
. . .

11. Pathophysiology of CHF
• Vasoconstriction: ↑’s the resistance against which
heart has to pump (i.e., ↑’s afterload), and may
therefore ↓ CO
• Na and water retention: ↑’s fluid volume, which
↑’s preload. If too much “stretch” (too much fluid)
→ ↓ strength of contraction and ↓’s CO
• Excessive tachycardia → ↓’d diastolic filling time →
↓’d ventricular filling → ↓’d SV and CO

13. Complications
• Arrythmias
• Heart valve problems
• Liver failure
• Kidney failure

14. DIAGNOSIS
• No single test is available to confirm the diagnosis of heart failure.
• The patient’s volume status should be documented by assessing the body
weight, JVP, and presence or absence of pulmonary congestion and
peripheral edema.
• Laboratory testing may assist in identification of disorders that cause or
worsen heart failure.
• The initial evaluation should include a complete blood count, serum
electrolytes (including magnesium), tests of renal and hepatic function,
urinalysis, lipid profile, chest x-ray, and a 12-lead electrocardiogram
(ECG).
• The echocardiogram also can determine the presence of systolic and/or
diastolic dysfunction and the left ventricular ejection fraction (LVEF).

15. Chronic Treatment of Heart Failure
• Correction of systemic factors
– Thyroid dysfunction
– Infections
– Uncontrolled diabetes
– Hypertension
• Lifestyle modification
– Lower salt intake
– Alcohol cessation
– Medication compliance
• Maximize medications
– Discontinue drugs that may contribute to heart
failure (NSAIDS, antiarrhythmics, calcium
channel blockers)

16. Order of Therapy
1. Loop diuretics
2. ACE inhibitor (or ARB if not tolerated)
3. Beta blockers
4. Digoxin
5. Hydralazine, Nitrate
6. Potassium sparing diuretcs

17. Diuretics
• Bolus administration of diuretics decreases preload by functional venodilation within 5 to 15
minutes and later (>20 minutes) via sodium and water excretion, thereby improving pulmonary
congestion.
• Loop diuretics
• Furosemide, buteminide
• For Fluid control, and to help relieve symptoms
• Potassium-sparing diuretics
• Spironolactone, eplerenone
• Help enhance diuresis
• Maintain potassium
• Shown to improve survival in CHF
• Although chronic diuretic therapy frequently is used in heart failure patients, it is not
mandatory and is required only in patients with peripheral edema and/or pulmonary
congestion.

18. ACE Inhibitor
• ACE inhibitors act upon the renin–angiotensin–aldosterone system, and
they reduce afterload by reducing the formation of angiotensin II, a
potent vasoconstrictor in the arterial system.
• These drugs also have an indirect effect on sodium and water retention by
inhibiting the release of aldosterone and vasopressin, thereby reducing
venous congestion and preload.
• Improve survival in patients with all severities of heart failure.
• Begin therapy low and titrate up as possible:
• Enalapril – 2.5 mg po BID
• Captopril – 6.25 mg po TID
• Lisinopril – 5 mg po QDaily
• If cannot tolerate, may try ARB

19. Beta Blocker therapy
• Formerly, β-blockers have been contraindicated in patients with heart
failure.
• However, the sympathetic neurohormonal overactivity that occurs in
response to the failing heart has been identified as a decisive factor in the
progression of ventricular dysfunction.
• The use of β-blockers is, therefore, recommended for all patients with
heart failure due to left ventricular systolic dysfunction, irrespective of
age and the degree of dysfunction.
• Certain Beta blockers (carvedilol, metoprolol, bisoprolol) can improve
overall and event free survival in NYHA class II to III HF, probably in class IV.

20. • Cause “reverse remodeling” of the left ventricle.
• Contraindicated:
– Heart rate <60 bpm
– Symptomatic bradycardia
– Signs of peripheral hypoperfusion
– COPD, asthma
– PR interval > 0.24 sec, 2nd or 3rd degree block

21. Hydralazine plus Nitrates
• Nitric oxide is released from the nitrate compound and
this in turn activates soluble guanylate cyclase in
vascular smooth muscle, leading to the vasodilatory
effect.
• Hydralazine has a direct action on arteriolar smooth
muscle to produce arterial vasodilation.
• Dosing:
– Hydralazine
– Started at 25 mg po TID, titrated up to 100 mg po TID
– Isosorbide dinitrate
– Started at 40 mg po TID/QID
• Decreased mortality, lower rates of hospitalization, and
improvement in quality of life.

22. Digoxin
• Given to patients with HF to control symptoms such as
fatigue, dyspnea, exercise intolerance
• Shown to significantly reduce hospitalization for heart failure,
but no benefit in terms of overall mortality.
• Digoxin doses should be adjusted to achieve plasma
concentrations of 0.5 to 1 ng/mL; higher plasma
concentrations are not associated with additional benefits but
may be associated with increased risk of toxicity.

23. • Digoxin exerts its positive inotropic effect by binding to sodium-
and potassium-activated adenosine triphosphatase (Na+,K+-
ATPase or sodium pump) Inhibition of Na+,K+- ATPase decreases
outward transport of sodium and leads to increased intracellular
sodium concentrations.
• Higher intracellular sodium concentrations favor calcium entry and
reduce calcium extrusion from the cell through effects on the
sodium-calcium exchanger.
• The result is increased storage of intracellular calcium in the
sarcoplasmic reticulum and, with each action potential, a greater
release of calcium to activate contractile elements and thus
increases contractility of heart.

25. Inotropic agents
• Acute heart failure may require the use of one or more inotropic
agents, particularly the sympathomimetic agents dobutamine and
dopamine, in an intravenous continuous infusion.
• With dopamine, low doses (0–2 μcg/kg/min) have a predominant
effect on dopamine receptors within the kidneys to improve urine
output, intermediate doses (2–5 μcg/kg/min) affect β1-receptors,
producing an inotropic effect, and high doses (10 μcg/kg/min) have
a predominant action on α-adrenoreceptors.

26. Other important medication in Heart Failure --
Statins
• Statin therapy is recommended in CHF for the
secondary prevention of cardiovascular
disease.
• Some studies have shown a possible benefit
specifically in HF with statin therapy
• Improved LVEF
• Reversal of ventricular remodeling
• Reduction in inflammatory markers (CRP, IL-6, TNF-
alphaII)

27. Meds to AVOID in heart failure
• NSAIDS
– Can cause worsening of preexisting HF
• Thiazolidinediones
– Include rosiglitazone (Avandia), and pioglitazone (Actos)
– Cause fluid retention that can exacerbate HF
• Metformin
– People with HF who take it are at increased risk of potentially
lethic lactic acidosis

31. TREATMENT OF ADVANCED/DECOMPENSATED HEART FAILURE