anticongestive heart failure Flashcards
Classification
- Acute/ chronic
- Systolic dysfunction: produced by inadequate contractile strength and stroke volume
Diastolic dysfunction: the heart does not relax enough to allow proper filling - New York Heart Association Functional classification: I – asymptomatic, II – mild, III –
moderate, IV - severe - Left heart failure/ right heart failure
symptoms and signs
- Fatigue, exercise intolerance, wheeze
- *Cyanosis (hypoxia)
- Peripheral edema of legs, ankles and other organs, ascites
- Pulmonary edema, shortness of breath (dyspnea), orthopnea, paroxysmal
nocturnal dyspnea*
diagnosis
Chest x-ray
* ECG and exercise stress test on a treadmill
* Echocardiography (ultrasound)
* Coronary arteriography (catheter)
* Computer Tomography Angiography
* Positron Emission Tomography (PET)
* Magnetic Resonance Imaging (MRI)
cardiac physiology review
1) CO
2) afterload
3) preload
anticongestive heart failure drugs
1) diuretics
2) beta blockers
3) anti RAAS
4) cardiac glycosides
5) vasodilator
natriuretic peptides inhibit Na+ reabsorptions
1) recombinant BNP; nesirtide
crug therapy
1) inotropic: increase cardiac contraction
2) acute heart failure
- intravenous diuretics, inotropic agents, phosphodiesterase inhibitors, vasodilators
3) chronic heart failure
- ACE inhibitors, beta receptors blockers, angiotensin receptor blockers, aldosterone antagonist, digoxin, diuretic
cardiac glycosides
1) digitalis: digoxin and digitoxin
2) Often used to treat congestive heart
failure and is also used to treat certain
arrhythmias (atrial flutter and fibrillation)
* Main cardiac effects of digitalis are:
1) Decrease of conduction of electrical impulses
through the AV node, making it a commonly used
antiarrhythmic agent to control the heart rate
during atrial fibrillation or atrial flutter.
2) Increase of force of contraction (inotropic) via
inhibition of the Na+/K+ ATPase pump
3) Increase of vagal activity via CNS
digoxin mechanism
Digoxin binds to the α-subunit of the Na+/
K+ ATPase pump. Inhibition of the Na+/K+
pump leads to increased intracellular Na+
levels and decreased extracellular Na+
levels. This causes an increase in the
length of Phase 4 of the cardiac action
potential, leading to a decrease in heart
rate
–
Inhibition of the
Na+/K+ pump leads to increased
intracellular Na+ levels and decreased
extracellular Na+ levels, which in turn
slows down the extrusion of Ca2+ and
increase the activity of Na+/ Ca2+
exchanger. Increased amounts of Ca2+
are then available, improving
contractility of the heart
-
Digoxin also increases vagal activity via its action on the central nervous
system, thus decreasing the conduction of electrical impulses through the
AV node. This is important for its clinical use in different arrhythmias
SA node
1) direct
- no effect at therapeutic dose
2) indirect
- no effect at therapeutic dose
AV node
1) direct
- increased refractory period
- decreased conduction velocity
2) indirect
- decreased conduction velocity
- increased refractory period
clinical use
Most common indications:
o Atrial fibrillation and atrial flutter with rapid ventricular response, to reduce
the ventricular rate
o The use of digoxin in congestive heart failure with sinus rhythm was once
standard, but is now controversial.
* Side effects and clinic problems
Action potential
o Narrow therapeutic index (the margin between
effectiveness and toxicity).
o Adverse effects are more common with low
potassium levels.
o EKG abnormalities: shortened QRS complex,
atrial or ventricular extra systoles, paroxysmal
atrial tachycardia with AV block, ventricular
tachycardia or fibrillation.
* Quinidine (IA) should not be used to treat digoxin induced arrhythmia (because
of increasing plasma digoxin concentration), Lidocaine or Phenytoin (IB) is
commonly used instead
Other medication/treatment
Milrinone
o Phosphodiesterase 3 (PDE3 hydrolyzes and
inactivates cAMP) inhibitors
o Increased cAMP enhances Ca2+ influx in the
cardiac muscle, increase cardiac contraction
(inotropic)
o Increased cAMP reduces vascular smooth
muscle contraction, vasodilation
o Used to treat acute heart failure
* Nesiritide (recombinant BNP)
* Left Ventricular Assist Devices (LVAD)
* Heart Transplant
* Life style
Dentists and Congestive heart failure drugs
Many medicines for treating congestive heart failure cause
xerostomia (dry mouth)
* Suggestions for dentists
1. Monitor vital signs at every appointment.
2. Look up any new drugs the patient is taking.
3. Evaluate patient anxiety and possible trauma from procedure.
4. Employ stress reduction protocols (shorter appointments, alternate treatment plan, etc.).
5. Position patient for easier breathing (semi-supine).
6. Avoid orthostatic hypotension by allowing patient to sit upright for two minutes before
standing.
7. Administer supplemental oxygen by nasal cannula or hood (3 - 5 ml flow rate) during treatment.
8. Careful use of vasoconstrictors, avoid epinephrine retraction cord.
9. Be mindful of sensitive gag reflex, avoid rubber dams, and be cautious with impressions,
radiographs, etc.