Congestive heartfailure

causes and pharmacotherapy

1. Congestive Heart Failure

2. Congestive Heart Failure
Definition
•Impaired cardiac pumping, heart is
unable to pump adequate amount of
blood to meet metabolic needs
•Associated with long-standing HTN and
CAD

3. Factors Affecting Cardiac Output
Cardiac Output
Preload
Afterload Contractility
Heart Rate Stroke Volume= X

4. Factors Affecting Cardiac Output
•Preload
–The volume of blood/amount of fiber stretch
in the ventricles at the end of diastole (i.e.,
before the next contraction)

5. Factors Affecting Cardiac Output
•Preload increases with:
•Fluid volume increases
•Vasoconstriction (“squeezes” blood from
vascular system into heart)
•Preload decreases with
•Fluid volume losses
•Vasodilation (able to “hold” more blood, therefore
less returning toheart)

6. End Diastolic Volume
(preload)
C
a
r
d
i
a
c

O
u
t
p
u
t

7. Factors Affecting Cardiac Output
•Afterload
–The resistance against which the ventricle must
pump. Excessive afterload = difficult to pump
blood → reduced CO/SV
–Afterload increased with:
•Hypertension
•Vasoconstriction
–Afterload decreased with:
•Vasodilation

8. Factors Affecting Cardiac Output
•Contractility
–Ability of the heart muscle to contract; relates
to the strength of contraction.

9. 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” (d/t too much
fluid) → ↓ strength of contraction and ↓’s CO
•Excessive tachycardia → ↓’d diastolic filling
time → ↓’d ventricular filling → ↓’d CO

10. Congestive Heart Failure
Risk Factors
•CAD
•Age
•HTN
•Obesity
•Cigarette smoking
•Diabetes mellitus
•High cholesterol

11. Congestive Heart Failure
Etiology
•May be caused by any interference with
normal mechanisms regulating cardiac
output (CO)
•Common causes
–HTN
–Myocardial infarction
–Dysrhythmias
–Valvular disorders

12. 2 Types of Heart Failure
Systolic Dysfunction
(Contraction) 2/3 of Patients
♥ The heart becomes weak
and enlarged
♥ The weakened heart
muscle can’t contract
♥ Not enough blood is
pumped from the
chambers
Diastolic Dysfunction
(Relaxation)
♥ Chambers don’t fill up so
less blood goes to the
lungs and body
♥ Stiff heart muscle can’t
relax
♥ Not enough blood fills the
chambers

13. What is an Ejection Fraction? (EF)
The amount of blood that pumps out of
the heart with each beat
♥ Normal EF = 50 – 65%
♥ Damaged Heart Muscle EF = 40%
♥ Potential Heart Transplant EF = 20%

14. When the EF is Abnormal
What Happens in the Body?
♥ Less blood goes to the brain that may make you
feel confused or dizzy
♥ Your lungs may fill up with fluid making you feel
short of breath
♥ Your kidneys may not be able to get rid of the
fluid
♥ Your belly, ankles and feet may swell up

15. Other Signs and Symptoms of CHF
♥ Extreme Fatigue
♥ Frequent Coughing
♥ Sudden Weight Gain
♥ Chest Pain or Pressure
♥ Nausea, Loss of Appetite or Bloating
♥ Decreased Urination

16. Acute Congestive Heart Failure
Clinical Manifestations
•Pulmonary edema
–Agitation
–Pale or cyanotic
–Cold
–Severe dyspnea
–Tachypnea
–Pink, frothy sputum

17. Chronic Congestive Heart Failure
Clinical Manifestations
•Fatigue
•Dyspnea
–Paroxysmal nocturnal dyspnea (PND)
•Tachycardia
•Edema – (lung, liver, abdomen, legs)
•Nocturia

18. Chronic Congestive Heart Failure
Clinical Manifestations
•Behavioral changes
–Restlessness, confusion, ¯ attention
•Chest pain (d/t ¯ CO and ↑ myocardial work)
•Weight changes (r/t fluid retention)
•Skin changes
–Dusky appearance

19. New York Heart Association
Functional Classification
Class I
No symptoms with
ordinary activity
Class II
Slight limitation of
physical activity
results in fatigue,
shortness of breath,
chest pain or
irregular heart beat

20. Class III
Marked limitation of
physical activity.
Comfortable at rest, but
less than ordinary
physical activity results
in fatigue, irregular
heart beat, pain or
shortness of breath
Class IV
Unable to carry out any
physical activity without
discomfort
All symptoms in class III
even at rest

21. Congestive Heart Failure
Diagnostic Studies
•Primary goal is to determine underlying
cause
–Physical exam
–Chest x-ray
–ECG
–ECHO

22. Pharmacotherapy
•Reduction of volume overload (reduce preload)
–Diuretics
•Ventricular unloading (reduce afterload)
–Acute: nitroglycerin, sodium nitroprusside
–Chronic: inhibit renin-angiotensin-aldosterone system,
diuretics, ACE inhibitors, angiotensin antagonists
–Beta-blockers (also reduce sympathetic activation)
•Inotropic interventions
–Acute: dobutamine
–Chronic: phosphodiesterase inhibitors, digitalis

23. 1.ACE inhibitors
2. Diuretics
3. Inotropic drugs
•Cardiac glycosides - Digitalis
• b-agonist (Dobutamine) &
• PDE inhibitors (Amirinone, milrinone)

24. 4. Vasodilators
•Arteriolar-Hydralzine, minoxidil
•Ca blockers- Nifedipine
•K openers- Nicorandil
•Venous-GTN
5. b-Adrenergic blockers – carveidilol,
metoprolol

25. Cardiac Disorders
Cardiac Glycosides
•Digitalis - One of the oldest drugs
- Effective in treating congestive heart
failure (CHF)
- peripheral & lung tissues become
congested = CHF

26. •CHF can be left sided or right sided
•Cardiac glycosides = digitalis glycosides
- inhibits the Na - K pump inc.
intracellular Ca
cardiac muscle fibers contract more
efficiently
- Digitalis = 3 effects on the heart 1) +
inotropic action (inc. myocard. contraction)
2) - chronotropic action (dec. HR) #) -
dromotropic action (dec. conduction of the
heart cells

27. SR
ATP
ADP
Ca
2+
Ca
2+
3Na
+
Contraction
NaCaX
ATPase
3Na
+
ATPase
2K
+
RyR
Digoxin
(-)
Ca
2+
Ca
2+

28. Net Effect
•Positive inotropic action (an
increase in the force and
velocity of myocardial systolic
contraction).
•A decrease in the degree of
activation of the sympathetic
nervous system and renin-
angiotensin system.
•Slowing of the heart rate and
decreased conduction velocity
through the AV node.

29. Pharmacokinetic Parameters
•Absorption
–After oral dosing:
•Onset of action in 0.5 – 2 hours
•Peak effect reached in 2 – 6 hours
•Distribution
–Skeletal and heart muscle, but not into adipose tissue
–Up to 25-30% is bound to plasma proteins
•Metabolism
–Follows first-order kinetics
–Limited metabolism via sugar hydrolysis and lactone ring reduction
–Half-life = 1-2 days
•Excretion
–60-80% excreted unchanged in urine
–Undergoes ACTIVE tubular secretion in the kidneys

30. •Action = inc. myocardial contraction (+
inotrophy),
and slows HR (- chronotropy), therefore regulating
the rate & rhythm of the heart
- Therapeutic serum levels = 0.5 - 2.0 ng/ml
•Use = moderate/severe systolic CHF, arrythmias
•SE = Dig. toxicity - bradycardia (pulse < 60),
anorexia, diarrhea, N&V, blurred vision, lethargy -
older adults more prone to toxicity
•DI - Other heart meds

31. Side Effects & Toxicities
•Yellow/green visual changes, halos around light
•N&V and diarrhea (50-75% of patients)
•Bradycardia (75-90% of patients)
•Fatigue, malaise, confusion, headache, etc.
•Anorexia

32. Clinical Considerations
•Doses must be individualized and depends on the type & severity of the
disease, age & weight of the patient, renal function, and concomitant
disease states
•Normal dosage range is 125 – 500 mcg (50 – 200 mcg capsules) a day in
a single dose
•Contraindications: Patients w/ ventricular fibrillation, renal impairment,
hypokalemia, hypomagnesemia, hypercalcemia, and pulmonary disease
•Patient must be advised not to take nonprescription cough or cold
medications, antacids, laxatives, or antidiarrheals without consulting the
pharmacist or physician
•Pregnancy category C