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HEART FAILURE
cardiac disorder that impairs the ability of the ventricle to deliver adequate quantities of blood to the metabolizing tissues during normal activity or at rest
CLASS I
CLASSES OF HEART FAILURE
degree of effort necessary to elicit HF symptoms equals to those that would limit normal individuals
CLASS II
CLASSES OF HEART FAILURE
symptoms occurs with ordinary exertion
CLASS III
CLASSES OF HEART FAILURE
symptoms occurs with less- than-ordinary exertion.
CLASS IV
CLASSES OF HEART FAILURE
Symptoms occurs while at rest
LOW OUTPUT
Metabolic demands are NORMAL but heart is unable to meet them
HIGH OUTPUT
Metabolic demands are INCREASED (hyperthyroidism anemia)and the heart is unable to meet them
DIASTOLIC DYSFUNCTION
Result of hypertrophy and stiffening of myocardium, reduced filling
Reduced CO, normal ejection fraction
Does not respond to inotropic drugs
SYSTOLIC DYSFUNCTION
• Reduced mechanical pumping action
Reduced CO and reduced ejection fraction (< 45%)
Results from MI
respond to inotropic drugs
PERIPHERAL EDEMA
RIGHT-SIDED FAILURE =
PULMONARY EDEMA
LEFT-SIDED FAILURE =
Tachycardia
Decreased exercise tolerance
Shortness of breath
Cardiomegaly
Signs and symptoms of all types of HF
CONCENTRIC CARDIAC HYPERTROPHY
do to protect heart it CHANGE THE SIZE AND SHAPE
FRANK-STARLING MECHANISM
– increased fiber dilation heightens the contractile force, which then increases the energy released.
IT LOOSEN
AFTERLOAD
– tension in ventricular muscles during contraction.
In the left ventricle,
this tension is determined by the amount of force needed to overcome pressure in the pulmonary artery.
PRELOAD
– force exerted on the ventricular muscle at the end of diastole that determines the degree of muscle fiber stretch.
Also known as ventricular end diastolic pressure; also a key factor in contractility
Antibiotics
Digoxin
can affect the concentration of digoxin
KIDNEY
BILE
Digoxin
Digitoxin
EXERTED
Cardiac glycosides (DIGOXIN, DIGITOXIN)
sodium pump.
MECHANISM OF ACTION
inhibit Na+/K+ ATPase, the membrane-bound transporter often called the
disorientation
hallucinations
Central nervous system effects
IN ERDERLY
Gynecomastia
is a rare effect
it is not certain whether this effect represents a peripheral estrogenic action of these steroid drugs or a manifestation of hypothalamic stimulation.
POSITIVE INOTROPIC EFFECTS
DEACTIVATION OF renin-angiotensin-aldosterone compensation
THERAPEUTIC EFFECTS of DIGOXIN
DIGOXIN
With narrow therapeutic index
available in tablet, injection, elixir and capsule forms.
0.5–1.5 ng/mL
DOSAGE AND ADMINISTRATION of Digoxin
Therapeutic plasma concentration
> 2 ng/mL
DOSAGE AND ADMINISTRATION of Digoxin
Toxic plasma concentration
0.25 (0.125–0.5) mg
DOSAGE AND ADMINISTRATION of Digoxin
Daily dose (slow loading or maintenance)
0.5–0.75 mg every 8 hours for three doses
DOSAGE AND ADMINISTRATION of Digoxin
Rapid digitalizing dose (rarely used)
QUINIDINE
RISK OF TOXICITY •increases with coadminstration of
DECREASE RENAL CLEARANCE OF DIGOXIN
potassium supplements
C. TREATMENT OF TOXICITY
If the patient is hypokalemic: Administer
lidocaine or phenytoin
C. TREATMENT OF TOXICITY
Arrhythmias
Cholestyramine
C. TREATMENT OF TOXICITY
binds to digitalis glycosides to prevent absorption of digitalis in the bile
purified digoxin Fab fragment antibodies.
DIGIbind
C. TREATMENT OF TOXICITY
Patients with very high serum digoxin levels
Diuretics
MOA: to reduce venous pressure and ventricular preload
GOAL: to reduce and eventually eliminate signs and
THIAZIDE diuretics
lose their effectiveness in HF patients with moderately impaired renal function
LOOP diuretics
increase sodium excretion to 20-25% of the filtered load
reverse pulmonary edema
POTASSIUM SPARING
Given to patients already on Digoxin or ACE inhibitors
Vasodilators
reduce pulmonary congestion effective in acute heart failure because they provide a reduction in preload (through venodilation), or reduction in afterload (through arteriolar dilation), or both
NITRO PRUSSIDE
Vasodilators
- provide potent dilation of both arteries and veins
HYDRA LAZNE
Vasodilators
decreases afterload and increases cardiac output.
PRA ZOSIN
Vasodilators
arteriovenous dilator
NITRATES
Vasodilators
— decreases preload
HYDRALAZINE + nitrosovasodilators
Combination of Vasodilators: reduce damaging remodeling of the heart
Reduce both preload and afterload
with ISOSORBIDE DINITRATE
Combination of Vasodilators: reduce damaging remodeling of the heart
reduce afterload
with NITROGLYCERIN
Combination of Vasodilators: reduce damaging remodeling of the heart
reduce preload
ACE INHIBITORS
first line agents in the treatment of HF beneficial effect on cardiac remodeling.
↓PVR ↓afterload ↓salt and water retention ↓ preload
added to a diuretic
Also indicated for patients with left ventricular dysfunction without symptoms of HF. for long-term management of chronic HF
Combine with a β-blocker, diuretic & digoxin Dose must be carefully titrated to the maximum allowable or tolerable dose
Oma patrilat
inhibits both ACE and neutral endopeptidase increase exercise tolerance
β-adrenergic blockers (bisoprolol, carvedilol, and metoprolol)
Used in stable severe heart failure used in conjunction with diuretics, ACE inhibitors and usually digoxin
should not be taken without diuretics in patients with a current or recent history of fluid retention
MONITOR bradycardia and the potential for heart block
INOTROPIC AGENTS
used in the emergency treatment of patients with HF and in patients refractory to or unable to take digitalis
. DOPAMINE (IV)
used in acute heart failure , ↑ TPR
DOBUTAMINE (IV)
↑ CO , ↓ in ventricular filling pressure
BIPYRIDINES
MOA: Inhibits phosphodiesterases , ↑ cAMP
INAMRINONE (IV)
INOTROPIC AGENTS
- Unstable in dextrose sol’n has both a positive inotropic effect and a vasodilating effect
MILRINONE (IV)
INOTROPIC AGENTS
ADR: hypotension, thrombocytopenia
NESIRITIDE (Natrecor®)
A synthetic brain natriuretic peptide (BNP) •approved for the IV treatment of patients with acutely decompensated HF associated with shortness of breath at rest or with minimal activity.
MOA: it binds to natriuretic peptide receptors in blood vessels, resulting in increased production in guanosine 3’5’ cGMP in target tissues, which mediates vasodilation
Natrecor®
NESIRITIDE
BN
ADR: Excessive hypotension
NESIRITIDE (Natrecor®)
ADR
Bosentan
competitive inhibition of endothelin
use in pulmonary HPN .
teratogenic and hepatotoxic
Levosimendan
sensitizes the troponin system to calcium inhibit PDE
Alis kiren
renin inhibition
Carperitide
ularitide
NATRIURETIC PEPTIDES
atrial natriuretic peptide (ANP)
urodilatin